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2. Angiotensin-converting enzyme inhibition and food restriction in diabetic mice do not correct the increased sensitivity for ischemia-reperfusion injury

Author

Van der Mieren Gerry, Nevelsteen Ines, Vanderper Annelies, Oosterlinck Wouter, Flameng Willem, and Herijgers Paul

Subjects
Ischemia/reperfusion, Diabetes mellitus, Metabolic syndrome, In vivo contractility, Infarct size, Diseases of the circulatory (Cardiovascular) system, RC666-701
Abstract

Abstract Background The number of patients with diabetes or the metabolic syndrome reaches epidemic proportions. On top of their diabetic cardiomyopathy, these patients experience frequent and severe cardiac ischemia-reperfusion (IR) insults, which further aggravate their degree of heart failure. Food restriction and angiotensin-converting enzyme inhibition (ACE-I) are standard therapies in these patients but the effects on cardiac IR injury have never been investigated. In this study, we tested the hypothesis that 1° food restriction and 2° ACE-I reduce infarct size and preserve cardiac contractility after IR injury in mouse models of diabetes and the metabolic syndrome. Methods C57Bl6/J wild type (WT) mice, leptin deficient ob/ob (model for type II diabetes) and double knock-out (LDLR-/-;ob/ob, further called DKO) mice with combined leptin and LDL-receptor deficiency (model for metabolic syndrome) were used. The effects of 12 weeks food restriction or ACE-I on infarct size and load-independent left ventricular contractility after 30 min regional cardiac ischemia were investigated. Differences between groups were analyzed for statistical significance by Student’s t-test or factorial ANOVA followed by a Fisher’s LSD post hoc test. Results Infarct size was larger in ob/ob and DKO versus WT. Twelve weeks of ACE-I improved pre-ischemic left ventricular contractility in ob/ob and DKO. Twelve weeks of food restriction, with a weight reduction of 35-40%, or ACE-I did not reduce the effect of IR. Conclusion ACE-I and food restriction do not correct the increased sensitivity for cardiac IR-injury in mouse models of type II diabetes and the metabolic syndrome.

Published
2012
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4. Substrate mapping of the left atrium in persistent atrial fibrillation: spatial correlation of localized complex conduction patterns in global charge-density maps to low-voltage areas in 3D contact bipolar voltage maps

Author

Chierchia, Gian-Battista, Sieira, Juan, Vanderper, Annelies, Osorio, Thiago Guimarães, Bala, Gezim, Stroker, Erwin, Brugada, Pedro, Al Houssari, Maysam, Cecchini, Federico, Mojica, Joerelle, Overeinder, Ingrid, Bisignani, Antonio, Mitraglia, Vincenzo, Boveda, Serge, Paparella, Gaetano, and de Asmundis, Carlo

Published
2021
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5. Long-term outcomes of the pentaspline pulsed-field ablation catheter for the treatment of paroxysmal atrial fibrillation: results of the prospective, multicentre FARA-Freedom Study

Author

Metzner, Andreas, primary, Fiala, Martin, additional, Vijgen, Johan, additional, Ouss, Alexandre, additional, Gunawardene, Melanie, additional, Hansen, Jim, additional, Kautzner, Josef, additional, Schmidt, Boris, additional, Duytschaever, Mattias, additional, Reichlin, Tobias, additional, Blaauw, Yuri, additional, Sommer, Philipp, additional, Vanderper, Annelies, additional, Achyutha, Anitha B, additional, Johnson, Madeline, additional, Raybuck, Jonathan D, additional, and Neuzil, Petr, additional

Published
2024
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6. AB-452675-4 CORONARY ARTERIAL SPASM DURING CAVO-TRICUSPID ISTHMUS ABLATION WITH A NOVEL FOCAL PULSED FIELD ABLATION CATHETER: FINDINGS FROM CORONARY ANGIOGRAPHY AND FRACTIONAL FLOW RESERVE MEASUREMENTS

Author

Malyshev, Yury, primary, Neuzil, Petr, additional, Petru, Jan, additional, Funasako, Moritoshi, additional, Kralovec, Stepan, additional, Skoda, Jan, additional, Schneider, Christopher, additional, Achyutha, Anitha, additional, Vanderper, Annelies, additional, Turagam, Mohit K., additional, and Reddy, Vivek Y., additional

Published
2023
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7. AB-452675-4 CORONARY ARTERIAL SPASM DURING CAVO-TRICUSPID ISTHMUS ABLATION WITH A NOVEL FOCAL PULSED FIELD ABLATION CATHETER: FINDINGS FROM CORONARY ANGIOGRAPHY AND FRACTIONAL FLOW RESERVE MEASUREMENTS

Author

Yury Malyshev, Petr Neuzil, Jan Petru, Moritoshi Funasako, Stepan Kralovec, Jan Skoda, Christopher Schneider, Anitha Achyutha, Annelies Vanderper, Mohit K. Turagam, and Vivek Y. Reddy

Subjects
Physiology (medical), Cardiology and Cardiovascular Medicine
Published
2023
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8. Hospital antibiotic prescribing patterns in adult patients according to the WHO Access, Watch and Reserve classification (AWaRe): results from a worldwide point prevalence survey in 69 countries

Author

Pauwels, Ines, Versporten, Ann, Drapier, Nico, Vlieghe, Erika, Goossens, Herman, Koraqi, Andi, Hoxha, Iris, Tafaj, Silva, Cornistein, Wanda, Quiros, Rodolfo, Hojman, Martin, Ghazaryan, Lilit, Horne, Kylie, Cairns, Kelly, Doukas, Fiona, Gottlieb, Thomas, Sermijn, Erica, Verhamme, Katia, Brands, Christiane, Van Herendael, Bruno, Filippin, Lorenzo, Vandewal, Wouter, Konopnicki, Deborah, Maillart, Evelyne, Teixeira Lopes, Liliana, Papin, Pauline, Smits, Ilse, Jansens, Hilde, Bartholomeus, Sofie, Van den Abeele, Anne-Marie, Steyaert, Sophia, Piette, Anne, Buyle, Franky, Cartuyvels, Reinoud, Jonckheere, Stijn, Wybo, Ingrid, Vanneste, Lorenz, Mathieu, Delphine, Firre, Eric, Westelinck, Veerle, Gadisseux, Philippe, Dugernier, Thierry, Bafort, Kristof, Gonissen, Viviane, Vanderper, Vanessa, Gabriels, Patrick, Weekers, Frank, Michel, Philippe, Van Liedekerke, Ann, Costers, Michiel, Catry, Boudewijn, Dedeic-Ljubovic, Amela, Gales, Ana C., Matos Porto, Ana Paula, Figueiredo Costa, Silvia, Keuleyan, Emma, Beidi, Apollinaire, Cissohko, Youssouph, Blakwe, Habsatou, Batchaya Basile, Ngassa, German, Greg J., Lutes, Sarah, Boswell, Jennifer, Mertz, Dominik, Nguyen, Tuyen, MacLaggan, Timothy, Landry, Daniel, Ang, Anita, Thirion, Daniel J.G., Frenette, Charles, Émond, Yannick, Roberts, Jacqueline, Chang, Sandra, Kosar, Justin, Valiquette, Louis, Dutrisac, Ginette, Afra, Kevin, McGeer, Allison, Carrier, Marie, Grant, Jennifer, Labarca, Jaime, Carvajal, Camila, Lin, HongYi, Wang, Qiang, Yang, Jing, Yang, Wenjie, Cortes, Jorge A., Villalobos-Vindas, Juan, Ramírez-Valverde, Carlos, Horvatic, Jasminka, Pristas, Irina, Paphitou, Niki, Rummukainen, Maija-Liisa, Froissart, Antoine, Vanhems, Philippe, Pagava, Karaman, Korinteli, Irma, Brandt, Tobias, Gaertner, Johannes, Enimil, Anthony, Roilides, Emmanuel, Hajdú, Edit, Sengupta, Sharmila, Singh, Sanjeev, Patil, Priyanka, Poojary, Aruna, Soltani, Jafar, Pouladfar, Gholamreza, Jafarpour, Zahra, Alinia, Cyrus, Ameen, Hadi, Fitzgerald, David, Paul, Mical, Maor, Yasmin, Strahilevitz, Jacob, Chowers, Michal, Temkin, Elizabeth, Luca, Arnoldo, Ishibashi, Noriomi, Gu, Yoshiaki, Darwish Elhajji, Feras, Karabukayeva, Aizhan, Raka, Denis, Kambaralieva, Baktygul, Zarakauska, Lelde, Zarb, Peter, Hernandez Chena, Blanca Estela, Gonzalez-Diaz, Esteban, Corona-Meléndez, JuanCarlos, Torres Erazo, Darwin Stalin, Loza-Jalil, Suria Elizabeth, Molina, Julio, Candelas, Jose Antonio, Mijovic, Gordana, Duborija-Kovacevic, Natasa, Jong, Eefje, Kluytmans, Jan, van Elzakker, Erika, Schweitzer, Valentijn, Davies, Nicola, Iregbu, Kenneth, Nwajiobi-Princewill, Philip, Nwafia, Ifeyinwa, Fasuyi, Temitayo, Aboderin, Aaron, Elikwu, Charles John, Fadeyi, Abayomi, Ola-Bello, Olafoyekemi, Oduyebo, Oyinlola, Adedosu, Akin Nelson, Ekuma, Agantem, Shaqiri, Erjona, Saleem, Zikria, De Los Reyes, Mari Rose, Tavares, Luis, Kim, Nam Joong, Rachina, Svetlana, Alharthi, Alwaleed R., Enani, Mushira, Faried, Osama, Mirghani, Mohamed, Carevic, Biljana, Radulovic, Lili, Dragovac, Gorana, Tan, Sock Hoon, Taljaard, Jantjie, Chibabhai, Vindana, Joiner, Jennifer, Caston, Juan Jose, Núñez-Núñez, María, Martínez-Marcos, Francisco Javier, Ojeda-Burgos, Guillermo, Menendez, Maria Dolores, Retamar, Pilar, Corzo, Juan E., Rattanaumpawan, Pinyo, Salou, Mounerou, Mnif, Basma, Oncul, Ahsen, Babigumira, Peter Ahabwe, Olweny, James, Marshall, Emily, McCorry, Ann, Aldeyab, Mamoon, Khanna, Priya, Gormley, Cairine, Maloney, Sara, Cooper, Mandelin, Blackburn, Laura, Gessner-Wharton, Mallory, Vu, Lam, Greer, Nickie, Gawrys, Gerard, Kronmann, Lisha, Rios, Edgar, Hudson, Melissa, Lindholm, David A., The Global-PPS network, Vriendenkring VUB, Clinical sciences, Microbiology and Infection Control, and Clinical Biology

Subjects
Adult, Microbiology (medical), Point prevalence survey, Latin Americans, education, Population, MEDLINE, World Health Organization, Essential medicines, Antibiotic prescribing, Anti-Infective Agents, Environmental health, Prevalence, Humans, AcademicSubjects/MED00740, Medicine, Pharmacology (medical), Medical prescription, Biology, Original Research, Pharmacology, education.field_of_study, Adult patients, business.industry, Pharmacology. Therapy, Hospitals, Anti-Bacterial Agents, Anti-Bacterial Agents/therapeutic use, AcademicSubjects/MED00290, Infectious Diseases, Human medicine, AcademicSubjects/MED00230, business
Abstract

ObjectivesThe WHO Access, Watch and Reserve (AWaRe) classification has been developed to support countries and hospitals in promoting rational use of antibiotics while improving access to these essential medicines. We aimed to describe patterns of worldwide antibiotic use according to the AWaRe classification in the adult inpatient population.MethodsThe Global Point Prevalence Survey on Antimicrobial Consumption and Resistance (Global-PPS) collects hospital antibiotic use data using a standardized PPS methodology. Global-PPS 2015, 2017 and 2018 data, collected by 664 hospitals in 69 countries, were categorized into AWaRe groups to calculate proportional AWaRe use, Access-to-Watch ratios and the most common indications for treatment with selected Watch antibiotics. Only prescriptions for systemic antibiotics on adult inpatient wards were analysed.ResultsRegional Access use ranged from 28.4% in West and Central Asia to 57.7% in Oceania, whereas Watch use was lowest in Oceania (41.3%) and highest in West and Central Asia (66.1%). Reserve use ranged from 0.03% in sub-Saharan Africa to 4.7% in Latin America. There were large differences in AWaRe prescribing at country level. Watch antibiotics were prescribed for a range of very different indications worldwide, both for therapeutic and prophylactic use.ConclusionsWe observed considerable variations in AWaRe prescribing and high use of Watch antibiotics, particularly in lower- and upper-middle-income countries, followed by high-income countries. The WHO AWaRe classification has an instrumental role to play in local and national stewardship activities to assess prescribing patterns and to inform and evaluate stewardship activities.

Published
2021
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9. Substrate mapping of the left atrium in persistent atrial fibrillation: spatial correlation of localized complex conduction patterns in global charge-density maps to low-voltage areas in 3D contact bipolar voltage maps

Author

Antonio Bisignani, Thiago Guimarães Osório, Juan Sieira, Gian-Battista Chierchia, Joerelle Mojica, Gezim Bala, Gaetano Paparella, Erwin Ströker, Pedro Brugada, Serge Boveda, Carlo de Asmundis, Vincenzo Mitraglia, Ingrid Overeinder, Annelies Vanderper, Maysam Al Houssari, Federico Cecchini, Cardiology, Clinical sciences, Heartrhythmmanagement, Faculty of Medicine and Pharmacy, Cardio-vascular diseases, and Medical Imaging

Subjects
medicine.medical_specialty, Spatial correlation, Substrate mapping, medicine.medical_treatment, 030204 cardiovascular system & hematology, Dipole density noncontact mapping, Low-voltage areas, Article, 03 medical and health sciences, 0302 clinical medicine, Heart Rate, Physiology (medical), Internal medicine, Atrial Fibrillation, medicine, Humans, Sinus rhythm, 030212 general & internal medicine, Heart Atria, Coronary sinus, business.industry, Charge density, Atrial fibrillation, Ablation, medicine.disease, SuperMap algorithm, 3D-mapping, Cardiology, Catheter Ablation, business, Cardiology and Cardiovascular Medicine, Electrophysiologic Techniques, Cardiac, Low voltage
Abstract

Purpose This study aimed to investigate the spatial relationship between low-voltage areas (LVAs) in bipolar voltage mapping (BVM) and localized complex conduction (LCC)-cores in a global, non-contact, charge-density-based imaging, and mapping system (AcM). Methods Patients with history of index PVI for PsAF and scheduled for a repeat ablation procedure for recurrence of the same arrhythmia were enrolled between August 2018 and February 2020. All patients underwent both substrate mappings of the left atrium (LA) with the CARTO 3D map-ping system and with AcM. Results Ten patients where included in our analysis. All presented with persistency of PVI in all veins at the moment of repeat procedure. There was no linear relationship in BVM maps between SR and CSd (correlation coefficient 0.31 ± 0.15), SR and CSp (0.36 ± 0.12) and CSd and CSp (0.43 ± 0.10). The % overlap of localized irregular activation (LIA), localized rotational activation (LRA) and Focal (F) regions with LVA was lower at 0.2 mV compared to 0.5 mV (4.97 ± 7.39%, 3.27 ± 5.25%, 1.09 ± 1.92% and 12.59 ± 11.81%, 7.8 ± 9.20%, 4.62 ± 5.27%). Sensitivity and specificity are not significantly different when comparing composite maps with different LVA cut-offs. AURC was 0.46, 0.48, and 0.39 for LIA, LRA, and Focal, respectively. Conclusion Due to wave front direction dependency, LVAs mapped with BVM in sinus rhythm and during coronary sinus pacing only partially overlap in patients with PsAF. LCC-cores mapped during PsAF partially co-localize with LVAs.

Published
2021

10. Noncontact whole-chamber charge density mapping of the left ventricle: Preclinical evaluation in a sheep model

Author

F. Daniel Ramirez, Jeffrey R. Winterfield, Xinwei Shi, Derrick Chou, Dave Robinson, Nathan Angel, Pratik Shah, Tim Sorrell, Elyar Ghafoori, Annelies Vanderper, Leo Mariappan, Bruno Soré, Jean-Marc Peyrat, Virginie Loyer, Yosuke Nakatani, Hubert Cochet, and Pierre Jaïs

Subjects
Cicatrix, Sheep, Physiology (medical), Heart Ventricles, Tachycardia, Ventricular, Animals, Contrast Media, Arrhythmias, Cardiac, Gadolinium, Cardiology and Cardiovascular Medicine
Abstract

Conventional contact-based electroanatomic mapping is poorly suited for rapid or dynamic ventricular arrhythmias. Whole-chamber charge density (CD) mapping could efficiently characterize complex ventricular tachyarrhythmias and yield insights into their underlying mechanisms.The purpose of this study was to evaluate the feasibility and accuracy of noncontact whole-chamber left ventricular (LV) CD mapping and to characterize CD activation patterns during sinus rhythm, ventricular pacing, and ventricular fibrillation (VF).Ischemic scar as defined by CD amplitude thresholds was compared to late gadolinium enhancement criteria on magnetic resonance imaging using an iterative closest point algorithm. Electrograms recorded at sites of tissue contact were compared to the nearest noncontact CD-derived electrograms to calculate signal morphology cross-correlations and time differences. Regions of consistently slow conduction were examined relative to areas of scar and to localized irregular activation (LIA) during VF.Areas under receiver operating characteristic curves (AUCs) of CD-defined dense and total LV scar were 0.92 ± 0.03 and 0.87 ± 0.06, with accuracies of 0.86 ± 0.03 and 0.80 ± 0.05, respectively. Morphology cross-correlation between 8677 contact and corresponding noncontact electrograms was 0.93 ± 0.10, with a mean time difference of 2.5 ± 5.6 ms. Areas of consistently slow conduction tended to occur at scar borders and exhibited spatial agreement with LIA during VF (AUC 0.90 ± 0.02).Noncontact LV CD mapping can accurately delineate ischemic scar. CD-derived ventricular electrograms correlate strongly with conventional contact-based electrograms. Regions with consistently slow conduction are often at scar borders and tend to harbor LIA during VF.

Published
2021

13. B-AB01-03 HIGH-RESOLUTION REAL-TIME LEFT-VENTRICULAR ENDOCARDIAL ACTIVATION-REPOLARIZATION MAPPING IN AN IN-VIVO CANINE MODEL OF DRUG-INDUCED LONG-QT 1 SYNDROME AND TORSADES DE POINTES

Author

Nathan Angel, David J. Gallacher, Tim Corvi, Henk van der Linde, Rachel M.A. ter Bekke, Annelies Vanderper, and Paul G.A. Volders

Subjects
Drug, medicine.medical_specialty, business.industry, media_common.quotation_subject, High resolution, Torsades de pointes, medicine.disease, In vivo, Physiology (medical), Internal medicine, medicine, Cardiology, Repolarization, Cardiology and Cardiovascular Medicine, business, Canine model, media_common
Published
2021
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19. Point prevalence survey of antimicrobial use and healthcare-associated infections in Belgian acute care hospitals : results of the Global-PPS and ECDC-PPS 2017

Author

Vandael, Eline, Latour, Katrien, Goossens, Herman, Magerman, Koen, Drapier, Nico, Catry, Boudewijn, Versporten, Ann, Andre, Marie, Aouachria, Samy, Aoun, Mickael, Bafort, Kristof, Bartholomeus, Sofie, Blumental, Sophie, Bothy, Anais, Brands, Christiane, Brassinne, Laetitia, Briquet, Caroline, Cartuyvels, Reinoud, Ceyssens, Clara, Cooreman, Sarah, Decleire, Pierre-Yves, Declercq, Philippe, De Cooman, Liesbeth, De Cuyper, Inge, Degraeve, Dirk, Delaere, Benedicte, Delvallee, Melanie, Desmedt, Marjoleine, Diaz, Victoria, Dragos, Ilisei, Dugernier, Thierry, Elsen, Elodie, Filippin, Lorenzo, Firre, Eric, Frans, Johan, Gabriels, Patrick, Gadisseux, Philippe, Gerard, Michele, Glibert, Bart, Goegebuer, Truus, Gonissen, Viviane, Harrouk, Antoine, Holemans, Xavier, Honore, Aline, Ide, Louis, Jansens, Hilde, Kidd, Francois, Koch, Annelies, Konopnicki, Deborah, Lefevre, Philippe, Lespagnard, Marc, Lorent, Sophie, Maillart, Evelyne, Mallet, Martine, Markowicz, Samuel, Mathieu, Delphine, Michel, Philippe, Noirhomme, Severine, Papin, Pauline, Piette, Anne, Pollet, Leen, Rossi, Camelia, Schatt, Patricia, Sermijn, Erica, Sterckx, Astrid, Steyaert, Sophia, Swinnen, Walter, Teixeira Lopes, Liliana, Thoelen, Inge, Turkova, Myriam, Van den Abeele, Anne-Marie, Van den Berg, Valerie, Van der beek, Danielle, Vanderper, Vanessa, Vandevelde, Marc, Vandewal, Wouter, Van Herendael, Bruno, Vanheule, Geert, Van Hoecke, Frederik, Van Kerkhoven, Dana, Van Liedekerke, Ann, Vanneste, Lorenz, Vekemans, Marc, Vercheval, Christelle, Verhamme, Katia, Verniest, Thessa, Westerlinck, Veerle, Wybo, Ingrid, Belgian Point Prevalence Survey, Swinnen, Walter/0000-0001-5387-149X, and Vriendenkring VUB

Subjects
Male, Antibiotics, Drug resistance, Antimicrobial Stewardship, Medical microbiology, Drug Utilization Review, Belgium, Risk Factors, Acute care, Antimicrobial consumption, Prevalence, Medicine, Pharmacology (medical), Pharmacology & Pharmacy, Point prevalence survey, Child, health care economics and organizations, Public, Environmental & Occupational Health, Medicine(all), Aged, 80 and over, Cross Infection, Pharmacology. Therapy, Middle Aged, Antimicrobial, Anti-Bacterial Agents, Infectious Diseases, Child, Preschool, Female, Life Sciences & Biomedicine, Microbiology (medical), Adult, medicine.medical_specialty, Adolescent, medicine.drug_class, education, Healthcare-associated infections, Microbiology, lcsh:Infectious and parasitic diseases, Young Adult, Internal medicine, Humans, lcsh:RC109-216, Medical prescription, Biology, Aged, Science & Technology, business.industry, Research, Public Health, Environmental and Occupational Health, Infant, Newborn, Infant, Généralités, medicine.disease, Health Surveys, Confidence interval, Pneumonia, Acute care hospitals, Human medicine, business
Abstract

Background: The point prevalence survey of healthcare-associated infections (HAIs) and antimicrobial use organized by the European Centre for Disease Prevention and Control (ECDC-PPS) and the Global Point Prevalence Survey of antimicrobial consumption (Global-PPS) were simultaneously performed in Belgian acute care hospitals in 2017. Methods: Belgian acute care hospitals were invited to participate in either the ECDC or Global-PPS. Hospital/ward/patient-level data were collected between September-December 2017. All patients present in the wards at 8 a.m. on the day of the PPS were included. The data of the ECDC and Global-PPS on antimicrobial consumption were pooled. Detailed data on HAIs were analysed for ECDC-PPS. Results: Overall, 110 Belgian acute care hospital sites participated in the ECDC and Global-PPS (countrywide participation rate: 81.4%, 28,007 patients). Overall, a crude prevalence of patients with at least one antimicrobial of 27.1% (95% confidence interval (CI) 26.5-27.6%) was found. The most frequently reported indications were pneumonia (23.2%), urinary tract infections (15.2%) and skin and soft tissue infections (11.9%). The reason for antimicrobial use was recorded for 81.9% of the prescriptions, a stop/review date for 40.8% and compliance with local antibiotic guidelines for 76.6%. In the ECDC-PPS, the crude prevalence of patients with at least one HAI was 7.3% (95%CI 6.8-7.7%). Most frequently reported HAIs were pneumonia (21.6%) and urinary tract infections (21.3%). Conclusions: HAI and antimicrobial use prevalence remained stable in comparison with the previous PPS (7.1% and 27.4% in 2011 and 2015, respectively). Belgian hospitals should be further stimulated to set local targets to improve antibiotic prescribing and reduce HAI., SCOPUS: ar.j, info:eu-repo/semantics/published

Published
2020

21. Glucose tolerance and left ventricular pressure-volume relationships in frequently used mouse strains

Author

Oosterlinck, Wouter, Vanderper, Annelies, Flameng, Willem, and Herijgers, Paul

Subjects
Physiological aspects, Research, Heart -- Physiological aspects -- Research, Blood glucose -- Physiological aspects -- Research, Blood sugar -- Physiological aspects -- Research
Abstract

1. Introduction Multiple transgenic mouse models have been and are being developed in cardiovascular research to study hypertension [1], diabetes [2], atherosclerosis [3], hypertrophic cardiomyopathy [4], heart failure [5], and [...], We investigated glucose tolerance and left ventricular contractile performance in 4 frequently used mouse strains (Swiss, C57BL/6J, DBA2, and BalbC) at 24 weeks. Glucose tolerance was tested by measuring blood glucose levels in time after intraperitoneal glucose injection (2 mg/g body weight). Left ventricular contractility was assessed by pressure-conductance analysis. Peak glucose levels and glucose area under the curve were higher (all P < .05) in C57BL/6J (418 ± 65mg/dL and 813 ± 100mg x h/dL) versus Swiss (237 ± 66mg/dL and 470 ± 126mg x h/dL), DBA2 (113 ± 20mg/dL and 304 ± 49mg x h/dL, P< .01), and BalbC mice (174 ± 55mg/dL and 416 ± 70mg x h/dL). Cardiac output was higher (all P< .05) in Swiss (14038 ± 4530 µL/min) versus C57BL/6J (10405 ± 2683 µL/min), DBA2 (10438 ± 3251 µL/min), and BalbC mice (8466 ± 3013 µL/min). Load-independent left ventricular contractility assessed as recruitable stroke work (PRSW) was comparable in all strains. In conclusion, glucose tolerance and load-dependent left ventricular performance parameters were different between 4 mice background strains, but PRSW was comparable.

Published
2011
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22. Contents Vol. 50, 2013

Author

Mauricio P. Boric, Maho Yamashita, An Van Den Bergh, Chihiro Horimai, William E. Sonntag, Mariela Puebla, Daniel Rojas-Líbano, Stephen J. Lewis, Xavier F. Figueroa, Daniel R. Gonzalez, Tadashi Yoshida, Kanigula Mubagwa, Yongliang Jiang, Gerry Van der Mieren, Matthew A. Boegehold, Pixin Ran, Juan Pablo Acevedo, Nicole M. Ashpole, Annelies Vanderper, Zoltan Ungvari, Tom P. Robertson, Paul Herijgers, Tristan H. Lewis, Yong Woo Lee, Xing Wen, Gongyong Peng, Stephen P. Chelko, Druckerei Stückle, Matsuhiko Hayashi, Chad W. Schmiedt, Yumin Zhou, Hidde Bult, Satz Mengensatzproduktion, Ines Nevelsteen, Guoping Hu, Yu Shi, Anna Csiszar, Junie P. Warrington, and Walter N. Durán

Subjects
Physiology, Cardiology and Cardiovascular Medicine
Published
2013
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23. Poster session 1

Author

J. Schlueter, T. Brand, D. J. Henderson, V. Boczonadi, P. Humbert, B. Chaudhry, D. Sedmera, J. Svatunkova, R. Kockova, B. Sankova, C. Lopez Sanchez, D. Franco, A. Aranega, V. Garcia-Martinez, E. Demina, V. Miroshikova, A. Denisenko, A. Schwarzman, F. Sanchez-Cabo, C. Torroja, A. Benguria, R. Buchan, P. Srivastava, F. Martinez, P. Barton, S. Cook, A. Dopazo, E. Lara-Pezzi, H. Rai, S. Kumar, A. K. Sharma, S. Mastana, A. Kapoor, C. M. Pandey, S. Agrawal, N. Sinha, J. Lipkova, M. Goldbergova, J. Parenica, J. Bienertova Vasku, A. Vasku, P. Kala, J. Spinar, L. Perez-Cabornero, D. Cantalapiedra, A. Forteza, R. Saez-Villaverde, J. Zumalde, V. Fernandez-Pedrosa, S. Zuniga-Trejos, M. Gil-Borja, M. Lazaro, S. Santillan, M. Costa, N. Cortez-Dias, P. Carrilho-Ferreira, D. Silva, C. Jorge, R. Placido, C. Calisto, M. Fiuza, A. Nunes Diogo, F. J. Enguita, H. H. W. Sillje, B. Lu, H. Yu, M. Zwartbol, W. P. Ruifrok, W. H. Van Gilst, R. A. De Boer, D. Zaliaduonyte-Peksiene, S. Simonyte, V. Lesauskaite, J. Vaskelyte, V. Mizariene, R. Zaliunas, W. Tigchelaar, E. Barlaka, A. Lazou, C. Del Giudice, E. Cipolletta, A. Anastasio, G. Santulli, M. Rusciano, A. S. Maione, P. Campiglia, M. Illario, B. Trimarco, G. Iaccarino, G. A. Frentzou, M. J. Drinkhill, N. A. Turner, S. G. Ball, J. F. X. Ainscough, L. Bertrand, F. Mailleux, J. Hammond, A. Ginion, L. Hue, J. L. Balligand, S. Horman, J. L. Vanoverschelde, C. Beauloye, B. Demeulder, S. L. Puhl, A. Mueller, Y. Devaux, D. R. Wagner, K. Roemer, M. Boehm, C. Maack, D. Miranda-Silva, I. Falcao-Pires, N. Goncalves, D. Moreira-Goncalves, A. F. Leite-Moreira, F. Mraiche, L. Fliegel, J. Xue, G. G. Haddad, L. C. Hsiao, C. Carr, Z. F. Cui, K. Clarke, M. A. D'amico, P. Izzicupo, A. Di Fonso, A. Bascelli, S. Gallina, A. Di Baldassarre, C. Silvestre, P. Fernandez, O. M. Pello, C. Indolfi, F. Civeira, R. Hutter, B. Ibanez, J. Chaves, J. Martinez-Gonzalez, V. Andres Garcia, A. Zabirnik, N. Smolina, A. Malashicheva, E. Omelchenko, T. Sejersen, A. Kostareva, C. Noack, M. P. Zafiriou, A. Renger, R. Dietz, H. J. Schaeffer, M. B. Bergmann, C. Zelarayan, S. Van Linthout, K. Miteva, M. P. Becher, M. Haag, J. Ringe, H.-P. schultheiss, M. Sittinger, C. Tschoepe, T. Kakuchaya, L. Bockeria, E. Golukhova, M. Eremeeva, N. Chigogidze, I. Aslanidi, I. Shurupova, A. Svobodov, A. A. Ramkisoensing, D. A. Pijnappels, J. Swildens, M. J. Goumans, M. J. Schalij, A. A. F. De Vries, D. E. Atsma, A. Gomes, G. M. Costa, C. A. Cordeiro, A. Matsuada, L. B. Rosario, A. P. Freire, M. Bousquenaud, M. Rolland-Turner, F. Maskali, L. Zhang, P. Y. Marie, F. Azuaje, A. J. Smith, G. M. Ellison, C. D. Waring, S. Purushothaman, D. Torella, B. Nadal-Ginard, M. H. Van Marion, D. W. J. Van Der Schaft, M.-J. Goumans, F. P. T. Baaijens, C. V. C. Bouten, N. Kraenkel, K. Kuschnerus, M. Mueller, T. Speer, S. Briand, M. Bader, P. Madeddu, T. F. Luescher, U. Landmesser, A. Papalamprou, C. Vicinanza, D. F. Goldspink, M. Noseda, S. J. Mcsweeney, T. Leja, E. Belian, I. Macaulay, F. Al-Beidh, S. Koenemann, M. S. Abreu Pavia, S. E. Jacobsen, M. D. Schneider, G. Foldes, Z. Bagyura, Z. Lendvai, D. Mathe, T. Nemeth, J. Skopal, I. Foldes, B. Merkely, S. E. Harding, A. J. Candasamy, R. S. Haworth, A. Boguslavsky, F. Cuello, M. J. Shattock, M. Mayr, M. Gautel, M. Avkiran, P. Leszek, B. Sochanowicz, M. Szperl, P. Kolsut, K. Brzoska, W. Piotrowski, T. Rywik, B. Danko, J. Rozanski, M. Kruszewski, N. Bouteldja, R. J. Woodman, C. L. Hewitson, E. Domingo, J. A. Barbara, A. A. Mangoni, R. Carnicer Hijazo, A. B. Hale, X. Liu, S. Suffredini, J. K. Bendall, G. B. S. Lim, N. J. Alp, K. M. Channon, B. Casadei, L. R. Moltzau, J. M. Aronsen, S. Meier, I. Sjaastad, T. Skomedal, J.-B. Osnes, F. O. Levy, E. Qvigstad, P. T. Wright, L. M. K. Pannell, A. R. Lyon, J. Gorelik, A. Guellich, S. F. Vatner, R. Fischmeister, B. Manoury, E. Dubois, J. Hamelet, A. Vanderper, P. Herijgers, D. Langin, F. Gartner, J. Gummert, H. Milting, G. Euler, M. Priess, J. Heger, T. Noll, R. Schulz, T. Doi, T. Akagami, T. Naka, T. Masuyama, M. Ohyanagi, M. Massaro, E. Scoditti, M. Pellegrino, M. A. Carluccio, C. Martines, C. Storelli, R. De Caterina, M. Falck-Hansen, M. E. Goddard, J. E. Cole, N. Astola, A. J. Cross, R. Krams, C. Monaco, M. F. Corsten, W. Verhesen, A. P. Papageorgiou, P. Carai, M. Lindow, S. Obad, G. Summer, L. De Rijck, S. Coort, M. Hazebroek, R. Van Leeuwen, M. Gijbels, M. P. J. De Winther, F. R. M. Stassen, S. Kauppinen, B. Schroen, S. Heymans, Z. Husti, V. Juhasz, L. Virag, A. Kristof, I. Koncz, T. Szel, I. Baczko, N. Jost, J. G. Y. Papp, A. Varro, A. Ghigo, A. Perino, F. Damilano, J. Leroy, V. O. Nikolaev, W. Richter, M. Conti, G. Vandecasteele, E. Hirsch, R. Ang, S. Sebastian, A. Ludwig, L. Birnbaumer, A. Tinker, E. A. Ertel, R. Sube, A. Opel, C. L-H Huang, A. Grace, N. Tribulova, J. Radosinska, B. Bacova, T. Benova, V. Knezl, J. Slezak, T. A. Matsuyama, T. Tanaka, T. Adachi, Y. Jiang, H. Ishibashi-Ueda, T. Takamatsu, J. Kornej, C. Reihardt, J. Kosiuk, A. Arya, G. Hindricks, V. Adams, D. Husser, A. Bollmann, S. Severi, M. Fantini, E. Ravagli, L. A. Charawi, D. Difrancesco, C. Poulet, L. Lu, U. R. Ravens, M. Hoch, T. Koenig, A. Gardiwal, B. Stapel, S. Erschow, A. Froese, B. Weinhold, R. Gerardy-Schahn, G. Klein, D. Hilfiker-Kleiner, K. Chinda, S. Palee, S. Surinkaew, M. Phornphutkul, S. Chattipakorn, N. Chattipakorn, B. Tuana, Z. Kohajda, A. A. Kristof, C. Corici, F. Fulop, N. L. Jost, V. Szuts, D. Menesi, G. L. Puskas, A. Zvara, N. Houshmand, J. G. Papp, N. Al-Shanti, M. Hancock, A. Venturini, C. Stewart, R. Ascione, G. Angelini, M.-S. Suleiman, A. Gonzalez-Tendero, I. Torre, F. Crispi, E. Gratacos, T. Tzanavari, E. Varela, A. Economides, S. Theocharis, C. Pantos, D. V. Cokkinos, A. Karalis, P. Hecker, V. Lionetti, W. C. Stanley, C. Ferrara, N. Piroddi, B. Scellini, C. Ferrantini, V. Sequiera, C. Remedios, L. Carrier, C. Tesi, J. Van Der Velden, C. Poggesi, V. Kooij, G. J. M. Stienen, D. Dooijes, s. Marston, C. Redwood, C. Dos Remedios, I. Diakonov, S. Tokar, M. Sikkel, S. Schlossarek, M. Sauer, A. Papageorgiou, S. Velthuis, E. Lutgens, M. Swinnen, N. Van Rooijen, J. Kzhyshkowska, P. Carmeliet, P. Garcia-Canadilla, F. Garcia-Garcia, I. Iruretagoiena, J. Dopazo, I. Amat-Roldan, M. H. Zhang, Y. H. Zhang, C. E. Sears, B. Wojtas, A. Llach, L. Hove-Madsen, V. Spinelli, L. Sartiani, M. Bucciantini, R. Coppini, E. Russo, A. Mugelli, E. Cerbai, M. Stefani, M. Ibrahim, P. Kukadia, M. Navaratnarajah, U. Siedlecka, C. Van Doorn, M. Yacoub, C. Terracciano, W. Song, N. Curtin, R. Woledge, S. Marston, M. Balteau, N. Tajeddine, G. Behets-Wydemans, C. Dessy, P. Gailly, W. J. Van Der Laarse, S. J. P. Bogaards, D. Van Groen, Y. Y. Wong, I. Schalij, A. Vonk Noordegraaf, F. M. Faz, B. Littlejohns, P. Pasdois, A. P. Halestrap, G. D. Angelini, S. Lemoine, V. Jaspard-Vinassa, F. Vigneron, P. Dos Santos, M. Popescu, A. Vlad, G. Isvoranu, L. Suciu, B. Marinescu, D. Dimulescu, L. Zagrean, P. W. M. Kleikers, K. Wingler, K. Radermacher, A. Sydykov, H. A. Ghofrani, N. Weissmann, H. H. W. Schmidt, A. Poddubnaya, K. E. M. Khurs, S. O. G. Smolenskaya, G. Szucs, Z. Murlasits, S. Torok, G. F. Kocsis, T. Csont, C. Csonka, P. Ferdinandy, R. Dongworth, D. M. Yellon, D. J. Hausenloy, Y. Y. Chen, W. S. Lian, C. F. Cheng, K. H. Khoo, T. C. Meng, G. Youcef, E. Belaidi, L. Fazal, M. P. Vinvent, D. De Paulis, G. Zadigue, C. Richer-Giudicelli, F. Alhenc-Gelas, M. Ovize, A. Pizard, R. Cal, J. Castellano, J. Farre, G. Vilahur, L. Badimon, V. Llorente-Cortes, H. Naz, M. Gharanei, C. Mee, H. Maddock, A. Hussain, O. Pisarenko, V. Shulzhenko, L. Serebryakova, I. Studneva, Y. Pelogeykina, D. Khatri, O. Tskitishvili, E. Barnucz, G. Veres, P. Hegedus, T. Radovits, S. Korkmaz, S. Klein, R. Zoller, M. Karck, G. Szabo, S. Morel, M. A. Frias, C. Rosker, R. W. James, S. Rohr, B. R. Kwak, V. Braunersreuther, B. Foglia, F. Mach, E. Shantsila, S. Montoro-Garcia, L. D. Tapp, S. Apostolakis, B. J. Wrigley, G. Y. H. Lip, E. Sokolowska, K. Przyborowski, K. Kramkowski, W. Buczko, A. Mogielnicki, U. Simonsen, E. R. Hedegaard, B. D. Nielsen, A. Kun, A. Hughes, C. Kroigaard, S. Mogensen, O. Frobert, K. Ait Aissa, J. P. Max, D. Wahl, T. Lecompte, P. Lacolley, V. Regnault, A. Novakovic, M. Pavlovic, A. Vranic, P. Milojevic, I. Stojanovic, M. Jovic, D. Nenezic, N. Ugresic, Q. Yang, G. W. He, L. Calvier, P. Reboul, B. Martin-Fernandez, V. Lahera, F. Zannad, V. Cachofeiro, P. Rossignol, N. Lopez-Andres, V. K. Pulakazhi Venu, R. Baetta, A. Bonomo, A. F. Muro, A. Corsini, A. L. Catapano, G. D. Norata, L. E. Viiri, L. E. Full, T. J. Navin, A. Didangelos, I. Seppala, T. Lehtimaki, A. H. Davies, R. Wait, D. Sedding, P. Stieger, C. Thoelen, S. Fischer, J. M. Daniel, R. Widmer-Teske, K. T. Preissner, N. Alenina, L. A. Rabelo, M. Todiras, V. N. Souza, J. M. Penninger, R. A. Santos, I. A. Leonova, S. A. Boldueva, V. S. Feoktistova, O. V. Sirotkina, M. G. Kolesnichenko, Z. Springo, P. Toth, P. Cseplo, G. Szijjarto, A. Koller, S. Puthenkalam, M. K. Frey, I. M. Lang, R. Madonna, H. Shelat, Y. J. Geng, T. Ziegler, V. Pfetsch, J. Horstkotte, C. Schwab, I. Rohwedde, R. Hinkel, Q. Di, S. Dietzel, U. Deutsch, C. Kupatt, I. Ernens, B. Lenoir, O. Fortunato, A. Caporali, E. Sangalli, D. Cordella, M. Marchetti, G. Spinetti, C. Emanueli, G. Arderiu, E. Pena, M. J. Forteza, V. Bodi, S. Novella, C. Alguero, I. Trapero, I. Benet, C. Hermenegildo, J. Sanchis, F. J. Chorro, A. Nemeth, S. Szabados, A. Cziraki, E. Sulyok, I. G. Horvath, M. Rauh, W. Rascher, I. Sikharulidze, I. B. Bakhlishvili, J. T. T. Laitinen, J. P. Hytonen, O. Leppanen, J. Taavitsainen, A. Partanen, P. Korpisalo, S. Yla-Herttuala, J. Lonn, J. Hallstrom, T. Bengtsson, M. C. Guisasola, E. Dulin, S. Stojkovic, C. Kaun, G. Maurer, K. Huber, J. Wojta, S. Demyanets, T. B. Opstad, A. Pettersen, S. Aakra, H. Arnesen, I. Seljeflot, M. Borrell-Pages, C. Romero, A. Toso, M. Leoncini, L. Tanini, T. Pizzetti, F. Tropeano, M. Maioli, P. Casprini, F. Bellandi, R. F. Antunes, J. C. Kaski, I. E. Dumitriu, E. Wu, A. A. L. Tareen, M. Udovychenko, I. Rudyk, K. Riches, L. Franklin, A. Maqbool, J. Bond, M. L. Koschinsky, D. J. O'regan, K. E. Porter, I. R. Parepa, A. I. Suceveanu, A. Suceveanu, L. Mazilu, L. Cojocaru, A. Rusali, L. A. Tuta, E. Craiu, D. Lindner, C. Zietsch, H.-P. Schultheiss, C. Tschope, D. Westermann, M. Miana, E. Martinez, R. Jurado, C. Delgado, N. Gomez-Hurtado, A. Briones, J. Young, T. J. Geng, A. Brodehl, T. Schmidt, O. Smolenskaya, C. Stegemann, D. Byzov, I. Mikhaylova, N. Chizh, E. Pushkova, O. Synchykova, B. Sandomirsky, O. Freylikhman, O. Rotar, N. Chromova, E. Moguchaya, V. Ivanenko, E. Kolesova, A. Erina, M. Boyarinova, A. Konradi, S. D. Preston, D. Baskaran, A. M. Plonczak, K. Norita, S. V. De Noronha, M. N. Sheppard, A. Haghikia, S. F. Hill, M. Hoepfner, B. Nitzsche, M. Schrader, F. Zengerling, B. Hoffmann, A. Pries, S. Gao, J. T. Laitinen, S. Laidinen, H. Markkanen, H. Karvinen, V. Marjomaki, I. Vajanto, T. T. Rissanen, K. Alitalo, P. Mello Ferrao, M. C. Waghabi, L. R. Garzoni, J. Ritterhoff, C. Weidenhammer, M. Voelkers, W. H. Zimmermann, J. Rabinowitz, P. Most, S. C. Gordts, I. Muthuramu, F. Jacobs, E. Van Craeyveld, E. Nefyodova, B. De Geest, D. R. Tribuddharat, D. R. Sathitkarnmanee, M. R. Buddhisa, M. S. Suwannasaen, D. R. Silarat, D. R. Ngamsangsirisup, D. R. Hawrylowicz, D. R. Lertmemongkolchai, S. Rain, M. L. Handoko, N. Westerhof, A. Vonk-Noordegraaf, F. S. De Man, A. S. Iakovleva, O. A. Mirolyubova, A. Berezin, T. A. Samura, Suwannasaen, Tippayawat, Ngamsangsirisup, D. R. Sutra, Hawrylowicz, Lertmemongkolchai, L. M. Lima, M. G. Carvalho, D. R. G. Junqueira, M. O. Sousa, A. Zampetaki, P. Willeit, L. Tilling, I. Drozdov, M. Prokopi, A. Shah, C. Boulanger, P. Chowienczyk, S. Kiechl, S. H. V. Oliveira, V. Kirillova, E. Prosviryakov, C. T. M. Van Der Pouw Kraan, F. J. P. Bernink, J. M. Baggen, L. Timmers, A. M. Beek, M. Diamant, A. C. Van Rossum, N. Van Royen, A. J. G. Horrevoets, J. E. A. Appelman, A. Zyatenkov, L. S. Kokov, Y. U. D. Volynskiy, M. Krestjyaninov, V. I. Ruzov, A. V. Villar, E. Martinez-Laorden, A. Almela, M. A. Hurle, M. L. Laorden, N. Apaijai, M. K. Mcmullen, J. M. Whitehouse, G. Shine, and A. Towell

Subjects
Gerontology, Physiology, business.industry, Physiology (medical), Cancer research, Medicine, SCRIB gene, Cardiology and Cardiovascular Medicine, business
Published
2012
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24. Hypoxic Preconditioning Preserves Cardiac Contractility and Reduces Infarct Size In Vivo

Author

Annelies Vanderper, Willem Flameng, Gerry Van der Mieren, Paul Herijgers, An Van Den Bergh, and Ines Nevelsteen

Subjects
medicine.medical_specialty, Ejection fraction, business.industry, Ischemia, Diastole, Endogeny, medicine.disease, Contractility, Preload, Coronary occlusion, In vivo, Internal medicine, Anesthesia, Cardiology, Medicine, business
Abstract

Background: Preconditioning is a powerful endogenous mechanism to protect the heart against ischemic dam- age. The second window of preconditioning (SWOP) is therapeutically the most attractive, but is hard to achieve by local cardiac ischemia 24 hrs before the index ischemia in the many mice models for cardiovascular pathology, because of ex- cessive mortality during the two procedures or the period in between. Hypoxic preconditioning is an attractive alternative preconditioning stimulus. To date, the SWOP after hypoxic preconditioning has not been studied in mice concerning in- farct size reduction and preservation of left ventricular contractility in vivo. Aim: To determine whether transient hypoxia can induce a SWOP in vivo in mice. Methods: Hypoxic preconditioning was induced by 5 cycles of 6 minutes of 6% oxygen in 24-week-old wild type mice. Twenty-four hours later, a 30 minutes coronary occlusion was performed. After 1 hour of reperfusion, in vivo cardiac pressure-conductance catheterization was performed with determination of the load-dependent and load-independent pa- rameters. Infarct size was determined by TTC-staining. Sham procedures were used to obtain non-preconditioned con- trols. Results: There was no mortality with the hypoxic preconditioning protocol. The left ventricular contractile parameters ejection fraction, end-systolic elastance and preload recruitable stroke work were significantly better preserved after ischemia in the preconditioned group. Diastolic relaxation (tau) was also significantly better preserved. Infarct size was reduced to half that of the non-preconditioned group. Conclusion: Hypoxic preconditioning is a feasible stimulus to induce in vivo a second window of preconditioning in mice. Infarct size is reduced and cardiac contractility better preserved after 30 min regional ischemia in vivo by hypoxic precon- ditioning 24 hrs earlier.

Published
2008
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25. Enhanced expression of β3-adrenoceptors in cardiac myocytes attenuates neurohormone-induced hypertrophic remodeling through nitric oxide synthase

Author

Irina Lobysheva, Dominique Langin, Jean-Luc Balligand, A.C. Pouleur, Annelies Vanderper, Konrad R. Götz, Karima Jnaoui, Christophe Beauloye, Denise Hilfiker-Kleiner, Andreas Markl, Hrag Esfahani, Emilie Dubois-Deruy, Luc Bertrand, Guido Iaccarino, Joanna Hammond, Geneviève Tavernier, Paul Herijgers, Viacheslav O. Nikolaev, Julien Hamelet, Catharina Belge, Chantal Dessy, Boris Manoury, Belge, C., Hammond, J., Dubois-Deruy, E., Manoury, B., Hamelet, J., Beauloye, C., Markl, A., Pouleur, A. -C., Bertrand, L., Esfahani, H., Jnaoui, K., Gotz, K. R., Nikolaev, V. O., Vanderper, A., Herijgers, P., Lobysheva, I., Iaccarino, G., Hilfiker-Kleiner, D., Tavernier, G., Langin, D., Dessy, C., Balligand, J. -L., Institut de Recherche Expérimentale et Clinique (IREC), Université Catholique de Louvain = Catholic University of Louvain (UCL), Pole of Cardiovascular Pathology and Cliniques Universitaires Saint-Luc, Division of Cardiology and Pneumology, University of Göttingen - Georg-August-Universität Göttingen, Department of Cardiovascular Sciences, Department of Medicine and Surgery, Università degli Studi di Salerno (UNISA)-RCCS 'Multimedia', Molecular Cardiology, Medizinische Hochschule Hannover (MHH), Institut des Maladies Métaboliques et Cardiovasculaires (I2MC), Université Toulouse III - Paul Sabatier (UT3), Université Fédérale Toulouse Midi-Pyrénées-Université Fédérale Toulouse Midi-Pyrénées-Institut National de la Santé et de la Recherche Médicale (INSERM), Simon, Marie Francoise, Georg-August-University = Georg-August-Universität Göttingen, and Università degli Studi di Salerno = University of Salerno (UNISA)-RCCS 'Multimedia'

Subjects
MESH: Signal Transduction, Male, MESH: Myocytes, Cardiac, MESH: Neurotransmitter Agents, MESH: Isoproterenol, Muscle hypertrophy, Heart Ventricle, chemistry.chemical_compound, Mice, Cyclic GMP-Dependent Protein Kinase, MESH: Cyclic GMP-Dependent Protein Kinases, Myocyte, MESH: Cyclic GMP, MESH: Animals, Myocytes, Cardiac, Cyclic GMP, Cells, Cultured, Neurotransmitter Agents, biology, MESH: Hypertrophy, Ventricular Remodeling, Angiotensin II, Receptors, adrenergic, beta, Nitric oxide synthase, Catecholamine, MESH: Nitric Oxide Synthase, MESH: Angiotensin II, Signal transduction, Cardiology and Cardiovascular Medicine, MESH: Cells, Cultured, Human, Signal Transduction, medicine.medical_specialty, MESH: Mice, Transgenic, Heart Ventricles, MESH: Ventricular Remodeling, Mice, Transgenic, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, In Vitro Techniques, Nitric oxide, Neurotransmitter Agent, Physiology (medical), Internal medicine, medicine, Cyclic GMP-Dependent Protein Kinases, Animals, Humans, Ventricular remodeling, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, MESH: Mice, MESH: Humans, business.industry, Animal, In Vitro Technique, Isoproterenol, Hypertrophy, medicine.disease, MESH: Male, Disease Models, Animal, Endocrinology, chemistry, Receptors, Adrenergic, beta-3, biology.protein, MESH: Heart Ventricles, MESH: Disease Models, Animal, Nitric Oxide Synthase, business, MESH: Receptors, Adrenergic, beta-3, cGMP-dependent protein kinase
Abstract

Background— β1-2-adrenergic receptors (AR) are key regulators of cardiac contractility and remodeling in response to catecholamines. β3-AR expression is enhanced in diseased human myocardium, but its impact on remodeling is unknown. Methods and Results— Mice with cardiac myocyte-specific expression of human β3-AR (β3-TG) and wild-type (WT) littermates were used to compare myocardial remodeling in response to isoproterenol (Iso) or Angiotensin II (Ang II). β3-TG and WT had similar morphometric and hemodynamic parameters at baseline. β3-AR colocalized with caveolin-3, endothelial nitric oxide synthase (NOS) and neuronal NOS in adult transgenic myocytes, which constitutively produced more cyclic GMP, detected with a new transgenic FRET sensor. Iso and Ang II produced hypertrophy and fibrosis in WT mice, but not in β3-TG mice, which also had less re-expression of fetal genes and transforming growth factor β1. Protection from Iso-induced hypertrophy was reversed by nonspecific NOS inhibition at low dose Iso, and by preferential neuronal NOS inhibition at high-dose Iso. Adenoviral overexpression of β3-AR in isolated cardiac myocytes also increased NO production and attenuated hypertrophy to Iso and phenylephrine. Hypertrophy was restored on NOS or protein kinase G inhibition. Mechanistically, β3-AR overexpression inhibited phenylephrine-induced nuclear factor of activated T-cell activation. Conclusions— Cardiac-specific overexpression of β3-AR does not affect cardiac morphology at baseline but inhibits the hypertrophic response to neurohormonal stimulation in vivo and in vitro, through a NOS-mediated mechanism. Activation of the cardiac β3-AR pathway may provide future therapeutic avenues for the modulation of hypertrophic remodeling.

Published
2014
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26. HMGCoA reductase inhibition reverses myocardial fibrosis and diastolic dysfunction through AMP-activated protein kinase activation in a mouse model of metabolic syndrome

Author

Denise Hilfiker-Kleiner, Sandrine Horman, Jean-Luc Balligand, Tim Van Assche, Julien Hamelet, Christophe Beauloye, Andreas Markl, Marc van Bilsen, Gauthier Noppe, Nerea Hermida, Paul Herijgers, Annelies Vanderper, Fysiologie, and RS: CARIM School for Cardiovascular Diseases

Subjects
Leptin, AMPK, Cardiac output, Time Factors, Physiology, AMP-Activated Protein Kinases, Ventricular Function, Left, Mice, AMP-activated protein kinase, Diastole, Fibrosis, Myocardial fibrosis, Rosuvastatin Calcium, Cells, Cultured, Mice, Knockout, Sulfonamides, Ventricular Remodeling, Metabolic syndrome, Diastolic dysfunction, Cardiology and Cardiovascular Medicine, Procollagen, Signal Transduction, medicine.medical_specialty, Heart Diseases, Lysyl oxidase, Biology, Transfection, Collagen Type I, Transforming Growth Factor beta1, Physiology (medical), Internal medicine, medicine, Animals, Protein kinase A, Myocardium, Recovery of Function, Fibroblasts, medicine.disease, Actins, Rats, Enzyme Activation, Fluorobenzenes, Mice, Inbred C57BL, Disease Models, Animal, Procollagen peptidase, Pyrimidines, Endocrinology, Receptors, LDL, biology.protein, Hydroxymethylglutaryl-CoA Reductase Inhibitors
Abstract

AIMS: The metabolic syndrome (MS) leads to myocardial fibrosis (MF) and diastolic dysfunction. Statins have proven beneficial effects in MS, but their impact on cardiac remodelling is uncertain. We examined the effects and mechanisms of chronic statin treatment on cardiac remodelling, e.g. fibrosis and diastolic properties. METHODS AND RESULTS: We used a mouse model deficient in leptin and the LDL-receptor (DKO) that reproduces this MS phenotype. DKO mice (12 weeks) were treated with rosuvastatin (R) for 6 months vs. placebo. Morphometric and echocardiographic measurements showed that R reduced cardiac mass and increased left-ventricular end-diastolic diameter despite unchanged cardiomyocyte dimensions. Similarly, R had no effect on the hypertrophic response to neurohormones in isolated cardiomyocytes. Conversely, R reversed the age-dependent development of MF as well as mRNA expression of TGF-β1 and several pro-fibrotic markers (procollagen type I, its carboxy-terminal proteinase, Lysyl oxidase). R similarly inhibited the pro-fibrotic effects of TGF-β1 on procollagen type I, alpha Smooth Muscle Actin expression and migratory properties of cardiac fibroblasts in vitro. In parallel, R increased the activation of AMP-activated protein kinase (AMPK), a known inhibitor of fibrosis, in vivo and in vitro, and the anti-fibrotic effects of R were abrogated in fibroblasts transfected with AMPKα1/α2 siRNA. The reversal of MF by R in DKO mice was accompanied with improved diastolic properties assessed by P-V loop analysis (slope of EDPVR, dP/dt min and cardiac output). CONCLUSION: In this model of MS, statin treatment reverses myocardial remodelling and improves ventricular relaxation through AMPK-mediated anti-fibrotic effects.

Published
2013

27. Glucose Tolerance and Left Ventricular Pressure-Volume Relationships in Frequently Used Mouse Strains

Author

Willem Flameng, Wouter Oosterlinck, Paul Herijgers, and Annelies Vanderper

Subjects
medicine.medical_specialty, Cardiac output, Article Subject, Health, Toxicology and Mutagenesis, lcsh:Biotechnology, inbred strains, lcsh:Medicine, Mice, Inbred Strains, c57bl/6j mice, stiffness, Mice, Stroke work, Insulin resistance, Heart Rate, insulin resistance, fat, Internal medicine, lcsh:TP248.13-248.65, Heart rate, Ventricular Pressure, Genetics, medicine, Animals, Molecular Biology, plasma, density-lipoprotein receptor, Glucose tolerance test, medicine.diagnostic_test, business.industry, lcsh:R, Isoproterenol, Area under the curve, cholesterol, Stroke Volume, General Medicine, Glucose Tolerance Test, Left ventricular contractility, medicine.disease, Endocrinology, Ventricular pressure, Molecular Medicine, hyperglycemia, atherosclerosis, business, Injections, Intraperitoneal, Research Article, Biotechnology
Abstract

We investigated glucose tolerance and left ventricular contractile performance in 4 frequently used mouse strains (Swiss, C57BL/6J, DBA2, and BalbC) at 24 weeks. Glucose tolerance was tested by measuring blood glucose levels in time after intraperitoneal glucose injection (2 mg/g body weight). Left ventricular contractility was assessed by pressure-conductance analysis. Peak glucose levels and glucose area under the curve were higher (all P < .05) in C57BL/6J (418 +/- 65 mg/dL and 813 +/- 100 mg.h/dL) versus Swiss (237 +/- 66 mg/dL and 470 +/- 126 mg.h/dL), DBA2 (113 +/- 20 mg/dL and 304 +/- 49 mg.h/dL, P < .01), and BalbC mice (174 +/- 55 mg/dL and 416 +/- 70 mg.h/dL). Cardiac output was higher (all P < .05) in Swiss (14038 +/- 4530 mu L/min) versus C57BL/6J (10405 +/- 2683 mu L/min), DBA2 (10438 +/- 3251 mu L/min), and BalbC mice (8466 +/- 3013 mu L/min). Load-independent left ventricular contractility assessed as recruitable stroke work (PRSW) was comparable in all strains. In conclusion, glucose tolerance and load-dependent left ventricular performance parameters were different between 4 mice background strains, but PRSW was comparable. ispartof: Journal of Biomedicine and Biotechnology vol:2011 ispartof: location:United States status: published

Published
2011

28. Food-restriction in obese dyslipidaemic diabetic mice partially restores basal contractility but not contractile reserve

Author

Peter Carmeliet, An Van Den Bergh, Frank Wuytack, Paul Herijgers, Annelies Vanderper, Stefan Janssens, Peter Vangheluwe, Willem Flameng, and Paul Holvoet

Subjects
medicine.medical_specialty, Mice, Obese, Hyperlipidemias, Ventricular Function, Left, Muscle hypertrophy, Diabetes Mellitus, Experimental, Sarcoplasmic Reticulum Calcium-Transporting ATPases, Contractility, Mice, Afterload, Weight loss, Internal medicine, Weight Loss, medicine, Animals, Obesity, Mice, Knockout, business.industry, Myocardium, Cardiac muscle, Cardiac reserve, medicine.disease, Myocardial Contraction, Mice, Inbred C57BL, medicine.anatomical_structure, Endocrinology, Diabetes Mellitus, Type 2, Heart failure, cardiovascular system, Dobutamine, Calcium, medicine.symptom, Cardiology and Cardiovascular Medicine, business, Food Deprivation, medicine.drug
Abstract

Aims Weight reduction programmes in morbidly obese, diabetic, and hyperlipidaemic subjects usually improve cardiac load and subsequently reverse hypertrophy. However, their effect on contractile dysfunction and impaired cardiac functional reserve is unknown. Methods and results The effect of food-restriction-induced weight loss on in vivo cardiac contractility before and during beta-adrenergic stimulation was assessed using left ventricular pressure–volume analysis in a mouse model featuring obesity and Type II diabetes (ob/ob), obesity, Type II diabetes, atherogenic dyslipidaemia, and hypertension (LDLR−/−;ob/ob), or wild-type. In addition, sarcoendoplasmic reticulum (SR) Ca2+ reuptake, interstitial collagen accumulation, and aortic atherosclerosis were measured. Food-restriction resulted in a 54% lower weight. Weight loss largely normalized pre- and afterload in both ob/ob and LDLR−/−;ob/ob mice. Contractility and relaxation improved after weight loss, partly explained by improved SR Ca2+ reuptake. Ventricular–vascular stiffening, interstitial collagen accumulation, and aortic atherosclerosis were less in food-restricted than in free-fed LDLR−/−;ob/ob mice. In contrast, cardiac reserve was similarly impaired in free-fed and food-restricted ob/ob and LDLR−/−;ob/ob mice. Conclusion Food-restriction in obese diabetic mice leads to improved cardiac performance by diminishing cardiac load and by ameliorating the intrinsic contractile properties of the cardiac muscle. However, cardiac reserve under dobutamine stimulation did not increase.

Published
2009

29. Dyslipidaemia in type II diabetic mice does not aggravate contractile impairment but increases ventricular stiffness

Author

An Van Den Bergh, Willem Flameng, Annelies Vanderper, Frank Wuytack, Jean-Luc Balligand, Fanny Desjardins, Paul Holvoet, Paul Herijgers, Peter Vangheluwe, Wim Verreth, and Ines Nevelsteen

Subjects
Leptin, Male, medicine.medical_specialty, Physiology, Blood Pressure, Type 2 diabetes, Ventricular Function, Left, Sarcoplasmic Reticulum Calcium-Transporting ATPases, Mice, Physiology (medical), Internal medicine, Diabetic cardiomyopathy, Diabetes mellitus, medicine, Animals, Abdominal obesity, Dyslipidemias, Mice, Knockout, Leptin Deficiency, business.industry, Myocardium, medicine.disease, Myocardial Contraction, Mice, Inbred C57BL, Endocrinology, Diabetes Mellitus, Type 2, Receptors, LDL, Heart failure, Female, Metabolic syndrome, medicine.symptom, Cardiology and Cardiovascular Medicine, business
Abstract

AIMS: Type II diabetes, often associated with abdominal obesity, frequently leads to heart failure. Clinical and epidemiological evidence suggests that supplemental dyslipidaemia and hypertension, as clustered in the metabolic syndrome, aggravate the cardiovascular outcome. The differential impact of type II diabetes and the metabolic syndrome on left ventricular function, however, remains incompletely defined. METHODS AND RESULTS: We studied left ventricular function in vivo using pressure-volume analysis in obese diabetic mice with leptin deficiency (ob/ob) and obese diabetic dyslipidemic mice with combined leptin and low-density lipoprotein-receptor deficiency (DKO). ob/ob and DKO mice developed a diabetic cardiomyopathy, characterized by impaired contractility and relaxation, from the age of 24 weeks onwards. This was-at least partially-explained by increased apoptosis and disturbed Ca(2+) reuptake in the sarcoplasmic reticulum (SR) in both mouse models. DKO, but not ob/ob, developed increased end-diastolic ventricular stiffness, paralleled by increased left ventricular myocardial fibrosis. Cardiac output was preserved in ob/ob mice by favourable loading conditions, whereas it decreased in DKO mice. CONCLUSIONS: Type II diabetes in mice leads to impaired contractility and relaxation due to disturbed Ca(2+) reuptake in the SR, but only when dyslipidaemia and hypertension are superimposed does vascular-ventricular stiffening increase and left ventricular myocardial fibrosis develop. ispartof: Cardiovascular Research vol:77 issue:2 pages:371-379 ispartof: location:England status: published

Published
2008

30. Human beta-3 adrenoreceptor over-expression inhibits cardiac hypertrophy in vitro and in vivo

Author

UCL - Cliniques universitaires Saint-Luc, UCL - SSS/IREC - Institut de recherche expérimentale et clinique, UCL - SSS/IREC/FATH - Pôle de Pharmacologie et thérapeutique, UCL - (SLuc) Service de médecine interne générale, Hammond, Joanna, Balligand, Jean-Luc, Hamelet, Julien, Van Assche, T., Belge, Catharina, Vanderper, A., Langin, D., Herijgers, P., Conference on Frontiers in Cardiovascular Biology, UCL - Cliniques universitaires Saint-Luc, UCL - SSS/IREC - Institut de recherche expérimentale et clinique, UCL - SSS/IREC/FATH - Pôle de Pharmacologie et thérapeutique, UCL - (SLuc) Service de médecine interne générale, Hammond, Joanna, Balligand, Jean-Luc, Hamelet, Julien, Van Assche, T., Belge, Catharina, Vanderper, A., Langin, D., Herijgers, P., and Conference on Frontiers in Cardiovascular Biology

Published
2010

31. Food-restriction in OB/OB mice restores sarcoplasmic reticulum Ca2+ uptake, but not in vivo β-adrenergic responsiveness

Author

Frank Wuytack, An Van Den Bergh, Peter Vangheluwe, Annelies Vanderper, and Paul Herijgers

Subjects
Ca2 uptake, medicine.medical_specialty, Chemistry, Endoplasmic reticulum, medicine.disease, Ryanodine receptor 2, Food restriction, Contractility, Endocrinology, In vivo, Diabetes mellitus, Internal medicine, medicine, Metabolic syndrome, Cardiology and Cardiovascular Medicine, Molecular Biology
Published
2007
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32. Enhanced Expression of β3-Adrenoceptors in Cardiac Myocytes Attenuates Neurohormone-Induced Hypertrophic Remodeling Through Nitric Oxide Synthase

Author

Belge, Catharina, primary, Hammond, Joanna, additional, Dubois-Deruy, Emilie, additional, Manoury, Boris, additional, Hamelet, Julien, additional, Beauloye, Christophe, additional, Markl, Andreas, additional, Pouleur, Anne-Catherine, additional, Bertrand, Luc, additional, Esfahani, Hrag, additional, Jnaoui, Karima, additional, Götz, Konrad R., additional, Nikolaev, Viacheslav O., additional, Vanderper, Annelies, additional, Herijgers, Paul, additional, Lobysheva, Irina, additional, Iaccarino, Guido, additional, Hilfiker-Kleiner, Denise, additional, Tavernier, Geneviève, additional, Langin, Dominique, additional, Dessy, Chantal, additional, and Balligand, Jean-Luc, additional

Published
2014
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33. Dyslipidaemia in type II diabetic mice does not aggravate contractile impairment but increases ventricular stiffness.

Author

UCL - MD/MINT - Département de médecine interne, UCL - (SLuc) Service de médecine interne générale, Van den Bergh, An, Vanderper, Annelies, Vangheluwe, Peter, Desjardins, Fanny, Nevelsteen, Ines, Verreth, Wim, Wuytack, Frank, Holvoet, Paul, Flameng, Willem, Balligand, Jean-Luc, Herijgers, Paul, UCL - MD/MINT - Département de médecine interne, UCL - (SLuc) Service de médecine interne générale, Van den Bergh, An, Vanderper, Annelies, Vangheluwe, Peter, Desjardins, Fanny, Nevelsteen, Ines, Verreth, Wim, Wuytack, Frank, Holvoet, Paul, Flameng, Willem, Balligand, Jean-Luc, and Herijgers, Paul

Abstract

AIMS: Type II diabetes, often associated with abdominal obesity, frequently leads to heart failure. Clinical and epidemiological evidence suggests that supplemental dyslipidaemia and hypertension, as clustered in the metabolic syndrome, aggravate the cardiovascular outcome. The differential impact of type II diabetes and the metabolic syndrome on left ventricular function, however, remains incompletely defined. METHODS AND RESULTS: We studied left ventricular function in vivo using pressure-volume analysis in obese diabetic mice with leptin deficiency (ob/ob) and obese diabetic dyslipidemic mice with combined leptin and low-density lipoprotein-receptor deficiency (DKO). ob/ob and DKO mice developed a diabetic cardiomyopathy, characterized by impaired contractility and relaxation, from the age of 24 weeks onwards. This was-at least partially-explained by increased apoptosis and disturbed Ca(2+) reuptake in the sarcoplasmic reticulum (SR) in both mouse models. DKO, but not ob/ob, developed increased end-diastolic ventricular stiffness, paralleled by increased left ventricular myocardial fibrosis. Cardiac output was preserved in ob/ob mice by favourable loading conditions, whereas it decreased in DKO mice. CONCLUSIONS: Type II diabetes in mice leads to impaired contractility and relaxation due to disturbed Ca(2+) reuptake in the SR, but only when dyslipidaemia and hypertension are superimposed does vascular-ventricular stiffening increase and left ventricular myocardial fibrosis develop.

Published
2008

36. ACE-inhibition, but not weight reduction restores cardiomyocyte response to β-adrenergic stimulation in the metabolic syndrome

Author

Gerry Van der Mieren, Annelies Vanderper, Kanigula Mubagwa, An Van Den Bergh, Karin R. Sipido, Paul Herijgers, Virginie Bito, and Ines Nevelsteen

Subjects
Cardiac function curve, Male, medicine.medical_specialty, Mice, Obese, Stimulation, Angiotensin-Converting Enzyme Inhibitors, Contractility, Mice, Cardiomyocyte contractility, In vivo, Diabetic cardiomyopathy, Internal medicine, Weight Loss, Extracellular, Medicine, Animals, Myocytes, Cardiac, Calcium Signaling, β-adrenergic stimulation, ACE-inhibition, Cells, Cultured, Calcium signaling, Hypocaloric diet, Metabolic Syndrome, Mice, Knockout, business.industry, Adrenergic beta-Agonists, medicine.disease, Mice, Inbred C57BL, Endocrinology, Female, Metabolic syndrome, Cardiology and Cardiovascular Medicine, business, Research Article
Abstract

Background Diabetic cardiomyopathy is characterized by systolic and early diastolic ventricular dysfunction. In the metabolic syndrome (MS), ventricular stiffness is additionally increased in a later stage. It is unknown whether this is related to intrinsic cardiomyocyte dysfunction, extrinsic factors influencing cardiomyocyte contractility and/or cardiac function, or a combination of both. A first aim was to study cardiomyocyte contractility and Ca2+ handling in vitro in a mouse model of MS. A second aim was to investigate whether in vivo hypocaloric diet or ACE-inhibition (ACE-I) improved cardiomyocyte contractility in vitro, contractile reserve and Ca2+ handling. Methods This study was performed in LDL-receptor (LDLR−/−) and leptin-deficient (ob/ob), double knock-out mice (DKO), featuring obesity, type II diabetes, atherogenic dyslipidemia and hypertension. Single knock-out LDLR−/−, ob/ob and wild type mice were used as controls. Cellular contractility, Ca2+ handling and their response to in vivo treatment with diet or ACE-I were studied in isolated cardiomyocytes at baseline, during β-adrenergic stimulation or increased extracellular Ca2+, using field stimulation and patch-clamp. Results In untreated conditions, prolongation of contraction-relaxation cycle and altered Ca2+ handling are observed in MS. Response to increased extracellular Ca2+ and β-adrenergic stimulation is impaired and could not be rescued by weight loss. ACE-I restored impaired response to β-adrenergic stimulation in MS, but not the decreased response to increased extracellular Ca2+. Conclusions Cardiomyocyte contractility and β-adrenergic response are impaired in MS, due to alterations in cellular Ca2+ handling. ACE-I, but not weight loss, is able to restore cardiomyocyte response to β-adrenergic stimulation in MS.

Published
2013

37. Angiotensin-converting enzyme inhibition and food restriction restore delayed preconditioning in diabetic mice

Author

Annelies Vanderper, Wouter Oosterlinck, Ines Nevelsteen, Paul Herijgers, Gerry Van der Mieren, and Willem Flameng

Subjects
medicine.medical_specialty, Time Factors, Endocrinology, Diabetes and Metabolism, Ischemia, Mice, Obese, Preconditioning, Angiotensin-Converting Enzyme Inhibitors, Ischemia/reperfusion injury, Diabetes Mellitus, Experimental, Contractility, Mice, Diabetes mellitus, Internal medicine, medicine, Animals, Original Investigation, Myocardial protection, Caloric Restriction, Mice, Knockout, biology, business.industry, Leptin, Angiotensin-converting enzyme, medicine.disease, Metabolic syndrome, Mice, Inbred C57BL, Endocrinology, Ischemic Preconditioning, Myocardial, biology.protein, Ischemic preconditioning, Analysis of variance, business, Cardiology and Cardiovascular Medicine
Abstract

Background Classical and delayed preconditioning are powerful endogenous protection mechanisms against ischemia-reperfusion damage. However, it is still uncertain whether delayed preconditioning can effectively salvage myocardium in patients with co-morbidities, such as diabetes and the metabolic syndrome. We investigated delayed preconditioning in mice models of type II diabetes and the metabolic syndrome and investigated interventions to optimize the preconditioning potential. Methods Hypoxic preconditioning was induced in C57Bl6-mice (WT), leptin deficient ob/ob (model for type II diabetes) and double knock-out (DKO) mice with combined leptin and LDL-receptor deficiency (model for metabolic syndrome). Twenty-four hours later, 30 min of regional ischemia was followed by 60 min reperfusion. Left ventricular contractility and infarct size were studied. The effect of 12 weeks food restriction or angiotensin-converting enzyme inhibition (ACE-I) on this was investigated. Differences between groups were analyzed for statistical significance by student’s t-test or one-way ANOVA followed by a Fisher’s LSD post hoc test. Factorial ANOVA was used to determine the interaction term between preconditioning and treatments, followed by a Fisher’s LSD post hoc test. Two-way ANOVA was used to determine the relationship between infarct size and contractility (PRSW). A value of p Results Left ventricular contractility is reduced in ob/ob compared with WT and even further reduced in DKO. ACE-I improved contractility in ob/ob and DKO mice. After ischemia/reperfusion without preconditioning, infarct size was larger in DKO and ob/ob versus WT. Hypoxic preconditioning induced a strong protection in WT and a partial protection in ob/ob mice. The preconditioning potential was lost in DKO. Twelve weeks of food restriction or ACE-I restored the preconditioning potential in DKO and improved it in ob/ob. Conclusion Delayed preconditioning is restored by food restriction and ACE-I in case of type II diabetes and the metabolic syndrome.

Published
2013

38. Angiotensin-converting enzyme inhibition and food restriction in diabetic mice do not correct the increased sensitivity for ischemia-reperfusion injury

Author

Willem Flameng, Gerry Van der Mieren, Ines Nevelsteen, Annelies Vanderper, Wouter Oosterlinck, and Paul Herijgers

Subjects
Leptin, lcsh:Diseases of the circulatory (Cardiovascular) system, medicine.medical_specialty, Time Factors, Endocrinology, Diabetes and Metabolism, Myocardial Infarction, Ischemia/reperfusion, Mice, Obese, Angiotensin-Converting Enzyme Inhibitors, Myocardial Reperfusion Injury, Infarct size, Ventricular Function, Left, Contractility, Mice, Diabetes mellitus, KUL-CoE-Cardio, Diabetic cardiomyopathy, Internal medicine, medicine, Ventricular Pressure, Animals, Myocardial infarction, Original Investigation, Caloric Restriction, Metabolic Syndrome, Mice, Knockout, biology, business.industry, Myocardium, Angiotensin-converting enzyme, In vivo contractility, medicine.disease, Myocardial Contraction, Mice, Inbred C57BL, Disease Models, Animal, Endocrinology, Diabetes Mellitus, Type 2, Receptors, LDL, lcsh:RC666-701, Heart failure, biology.protein, Cardiology, Metabolic syndrome, Cardiology and Cardiovascular Medicine, business, Reperfusion injury, Biomarkers
Abstract

Background The number of patients with diabetes or the metabolic syndrome reaches epidemic proportions. On top of their diabetic cardiomyopathy, these patients experience frequent and severe cardiac ischemia-reperfusion (IR) insults, which further aggravate their degree of heart failure. Food restriction and angiotensin-converting enzyme inhibition (ACE-I) are standard therapies in these patients but the effects on cardiac IR injury have never been investigated. In this study, we tested the hypothesis that 1° food restriction and 2° ACE-I reduce infarct size and preserve cardiac contractility after IR injury in mouse models of diabetes and the metabolic syndrome. Methods C57Bl6/J wild type (WT) mice, leptin deficient ob/ob (model for type II diabetes) and double knock-out (LDLR-/-;ob/ob, further called DKO) mice with combined leptin and LDL-receptor deficiency (model for metabolic syndrome) were used. The effects of 12 weeks food restriction or ACE-I on infarct size and load-independent left ventricular contractility after 30 min regional cardiac ischemia were investigated. Differences between groups were analyzed for statistical significance by Student’s t-test or factorial ANOVA followed by a Fisher’s LSD post hoc test. Results Infarct size was larger in ob/ob and DKO versus WT. Twelve weeks of ACE-I improved pre-ischemic left ventricular contractility in ob/ob and DKO. Twelve weeks of food restriction, with a weight reduction of 35-40%, or ACE-I did not reduce the effect of IR. Conclusion ACE-I and food restriction do not correct the increased sensitivity for cardiac IR-injury in mouse models of type II diabetes and the metabolic syndrome.

Published
2012

39. Sunday, 18 July 2010

Author

Schuchardt, M., primary, Toelle, M., additional, Huang, T., additional, Wiedon, A., additional, Van Der Giet, M., additional, Mill, C., additional, George, S., additional, Jeremy, J., additional, Santulli, G., additional, Illario, M., additional, Cipolletta, E., additional, Sorriento, D., additional, Del Giudice, C., additional, Anastasio, A., additional, Trimarco, B., additional, Iaccarino, G., additional, Jobs, A., additional, Wagner, C., additional, Kurtz, A., additional, De Wit, C., additional, Koller, A., additional, Suvorava, T., additional, Weber, M., additional, Dao, V., additional, Kojda, G., additional, Tsaousi, A., additional, Lyon, C., additional, Williams, H., additional, Barth, N., additional, Loot, A., additional, Fleming, I., additional, Keul, P., additional, Lucke, S., additional, Graeler, M., additional, Heusch, G., additional, Levkau, B., additional, Biessen, E., additional, De Jager, S., additional, Bermudez-Pulgarin, B., additional, Bot, I., additional, Abia, R., additional, Van Berkel, T., additional, Renger, A., additional, Noack, C., additional, Zafiriou, M., additional, Dietz, R., additional, Bergmann, M., additional, Zelarayan, L., additional, Hammond, J., additional, Hamelet, J., additional, Van Assche, T., additional, Belge, C., additional, Vanderper, A., additional, Langin, D., additional, Herijgers, P., additional, Balligand, J., additional, Perrot, A., additional, Neubert, M., additional, Posch, M., additional, Oezcelik, C., additional, Waldmuller, S., additional, Berger, F., additional, Scheffold, T., additional, Bouvagnet, P., additional, Ozcelik, C., additional, Lebreiro, A., additional, Martins, E., additional, Lourenco, P., additional, Cruz, C., additional, Martins, M., additional, Bettencourt, P., additional, Maciel, M., additional, Abreu-Lima, C., additional, Pilichou, K., additional, Bauce, B., additional, Rampazzo, A., additional, Carturan, E., additional, Corrado, D., additional, Thiene, G., additional, Basso, C., additional, Piccini, I., additional, Fortmueller, L., additional, Kuhlmann, M., additional, Schaefers, M., additional, Carmeliet, P., additional, Kirchhof, P., additional, Fabritz, L., additional, Sanchez, J., additional, Rodriguez-Sinovas, A., additional, Agullo, E., additional, Garcia-Dorado, D., additional, Lymperopoulos, A., additional, Rengo, G., additional, Gao, E., additional, Zincarelli, C., additional, Koch, W., additional, Morgan, P., additional, Diez, A., additional, Perez, N., additional, Cingolani, H., additional, Zahradnikova, A., additional, Polakova, E., additional, Zahradnik, I., additional, Fluschnik, N., additional, Sossalla, S., additional, Ort, K., additional, Neef, S., additional, Hasenfuss, G., additional, Maier, L., additional, Weinert, S., additional, Poitz, D., additional, Herold, J., additional, Schmeisser, A., additional, Strasser, J., additional, Braun-Dullaeus, R., additional, Nazari-Jahantigh, M., additional, Weber, C., additional, Schober, A., additional, Leuner, A., additional, Eichhorn, B., additional, Ravens, U., additional, Morawietz, H., additional, Babes, E., additional, Babes, V., additional, Popescu, M., additional, Ardelean, A., additional, Rus, M., additional, Bustea, C., additional, Gwozdz, P., additional, Csanyi, G., additional, Luzak, B., additional, Gajda, M., additional, Mateuszuk, L., additional, Chmura-Skirlinska, A., additional, Watala, C., additional, Chlopicki, S., additional, Kierzkowska, I., additional, Sulicka, J., additional, Kwater, A., additional, Strach, M., additional, Surdacki, A., additional, Siedlar, M., additional, Grodzicki, T., additional, Olieslagers, S., additional, Pardali, L., additional, Tchaikovski, V., additional, Ten Dijke, P., additional, Waltenberger, J., additional, Renner, M., additional, Redwan, B., additional, Winter, M., additional, Panzenboeck, A., additional, Jakowitsch, J., additional, Sadushi-Kolici, R., additional, Bonderman, D., additional, Lang, I., additional, Toso, A., additional, Tanini, L., additional, Pizzetti, T., additional, Leoncini, M., additional, Maioli, M., additional, Tedeschi, D., additional, Oliviero, C., additional, Bellandi, F., additional, Casprini, P., additional, Amato, M., additional, Molins, B., additional, Pena, E., additional, Badimon, L., additional, Ferreiro Gutierrez, J., additional, Ueno, M., additional, Alissa, R., additional, Dharmashankar, K., additional, Capodanno, D., additional, Desai, B., additional, Bass, T., additional, Angiolillo, D., additional, Chabielska, E., additional, Gromotowicz, A., additional, Szemraj, J., additional, Stankiewicz, A., additional, Zakrzeska, A., additional, Mohammed, S., additional, Molla, F., additional, Soldo, A., additional, Russo, I., additional, Germano, G., additional, Balconi, G., additional, Staszewsky, L., additional, Latini, R., additional, Lynch, F., additional, Austin, C., additional, Prendergast, B., additional, Keenan, D., additional, Malik, R., additional, Izzard, A., additional, Heagerty, A., additional, Czikora, A., additional, Lizanecz, E., additional, Rutkai, I., additional, Boczan, J., additional, Porszasz, R., additional, Papp, Z., additional, Edes, I., additional, Toth, A., additional, Colantuoni, A., additional, Vagnani, S., additional, Lapi, D., additional, Maroz-Vadalazhskaya, N., additional, Koslov, I., additional, Shumavetz, V., additional, Glibovskaya, T., additional, Ostrovskiy, Y., additional, Koutsiaris, A., additional, Tachmitzi, S., additional, Kotoula, M., additional, Giannoukas, A., additional, Tsironi, E., additional, Darago, A., additional, Orosz, P., additional, Megyesi, Z., additional, Schudeja, S., additional, Matschke, K., additional, Deussen, A., additional, Castro, M., additional, Cena, J., additional, Walsh, M., additional, Schulz, R., additional, Poddar, K., additional, Rha, S., additional, Ramasamy, S., additional, Park, J., additional, Choi, C., additional, Seo, H., additional, Park, C., additional, Oh, D., additional, Almeida, J., additional, Pimenta, S., additional, Bernardes, J., additional, Machado, J., additional, Sabatasso, S., additional, Laissue, J., additional, Hlushchuk, R., additional, Brauer-Krisch, E., additional, Bravin, A., additional, Blattmann, H., additional, Michaud, K., additional, Djonov, V., additional, Hirschberg, K., additional, Tarcea, V., additional, Pali, S., additional, Korkmaz, S., additional, Loganathan, S., additional, Merkely, B., additional, Karck, M., additional, Szabo, G., additional, Pagliani, L., additional, Faggin, E., additional, Rattazzi, M., additional, Puato, M., additional, Presta, M., additional, Grego, F., additional, Deriu, G., additional, Pauletto, P., additional, Kaiser, R., additional, Albrecht, K., additional, Schgoer, W., additional, Theurl, M., additional, Beer, A., additional, Wiedemann, D., additional, Steger, C., additional, Bonaros, N., additional, Kirchmair, R., additional, Kharlamov, A., additional, Cabaravdic, M., additional, 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Published
2010
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43. Enhanced Expression of ß3-Adrenoceptors in Cardiac Myocytes Attenuates Neurohormone-Induced Hypertrophic Remodeling Through Nitric Oxide Synthase.

Author

Belge, Catharina, Hammond, Joanna, Dubois-Deruy, Emilie, Manoury, Boris, Hamelet, Julien, Beauloye, Christophe, Markl, Andreas, Pouleur, Anne-Catherine, Bertrand, Luc, Esfahani, Hrag, Jnaoui, Karima, Götz, Konrad R., Nikolaev, Viacheslav O., Vanderper, Annelies, Herijgers, Paul, Lobysheva, Irina, Iaccarino, Guido, Hiliker-Kleiner, Denise, Tavernier, Geneviève, and Langin, Dominique

Published
2014
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44. Angiotensin-converting enzyme inhibition and food restriction restore delayed preconditioning in diabetic mice.

Author

der Mieren, Gerry Van, Nevelsteen, Ines, Vanderper, Annelies, Oosterlinck, Wouter, Flameng, Willem, and Herijgers, Paul

Subjects
ANGIOTENSINS, ENZYME inhibitors, TYPE 2 diabetes, KNOCKOUT mice, MYOCARDIAL infarction, ANALYSIS of variance
Abstract

Background: Classical and delayed preconditioning are powerful endogenous protection mechanisms against ischemia-reperfusion damage. However, it is still uncertain whether delayed preconditioning can effectively salvage myocardium in patients with co-morbidities, such as diabetes and the metabolic syndrome. We investigated delayed preconditioning in mice models of type II diabetes and the metabolic syndrome and investigated interventions to optimize the preconditioning potential. Methods: Hypoxic preconditioning was induced in C57Bl6-mice (WT), leptin deficient ob/ob (model for type II diabetes) and double knock-out (DKO) mice with combined leptin and LDL-receptor deficiency (model for metabolic syndrome). Twenty-four hours later, 30 min of regional ischemia was followed by 60 min reperfusion. Left ventricular contractility and infarct size were studied. The effect of 12 weeks food restriction or angiotensinconverting enzyme inhibition (ACE-I) on this was investigated. Differences between groups were analyzed for statistical significance by student's t-test or one-way ANOVA followed by a Fisher's LSD post hoc test. Factorial ANOVA was used to determine the interaction term between preconditioning and treatments, followed by a Fisher's LSD post hoc test. Two-way ANOVA was used to determine the relationship between infarct size and contractility (PRSW). A value of p<0.05 was considered significant. Results: Left ventricular contractility is reduced in ob/ob compared with WT and even further reduced in DKO. ACE-I improved contractility in ob/ob and DKO mice. After ischemia/reperfusion without preconditioning, infarct size was larger in DKO and ob/ob versus WT. Hypoxic preconditioning induced a strong protection in WT and a partial protection in ob/ob mice. The preconditioning potential was lost in DKO. Twelve weeks of food restriction or ACE-I restored the preconditioning potential in DKO and improved it in ob/ob. Conclusion: Delayed preconditioning is restored by food restriction and ACE-I in case of type II diabetes and the metabolic syndrome. [ABSTRACT FROM AUTHOR]

Published
2013
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