Search

Your search keyword '"Liaudet L"' showing total 440 results
Start Over Author "Liaudet L"
440 results on '"Liaudet L"'

8. Physiological response to prone positioning in intubated adults with COVID-19 acute respiratory distress syndrome: a retrospective study

Author

Boffi, A., Ravenel, M., Lupieri, E., Schneider, A., Liaudet, L., Gonzalez, M., Chiche, J.D., and Piquilloud, L.

Subjects
Adult, Respiratory Distress Syndrome, Humans, Retrospective Studies, Prone Position, Respiration, Artificial, COVID-19/therapy, Respiratory Distress Syndrome/diagnosis, Respiratory Distress Syndrome/therapy, ARDS, Alveolo-arterial gradient, COVID-19, Dead space, Oxygenation, Prone position, Proning, Respiratory system compliance, Ventilatory ratio
Abstract

COVID-19 related acute respiratory distress syndrome (ARDS) has specific characteristics compared to ARDS in other populations. Proning is recommended by analogy with other forms of ARDS, but few data are available regarding its physiological effects in this population. This study aimed to assess the effects of proning on oxygenation parameters (PaO 2 /FiO 2 and alveolo-arterial gradient (Aa-gradient)), blood gas analysis, ventilatory ratio (VR), respiratory system compliance (C RS ) and estimated dead space fraction (V D /V T HB). We also looked for variables associated with treatment failure. Retrospective monocentric study of intubated COVID-19 ARDS patients managed with an early intubation, low to moderate positive end-expiratory pressure and early proning strategy hospitalized from March 6 to April 30 2020. Blood gas analysis, PaO 2 /FiO 2 , Aa-gradient, VR, C RS and V D /V T HB were compared before and at the end of each proning session with paired t-tests or Wilcoxon tests (p < 0.05 considered as significant). Proportions were assessed using Fischer exact test or Chi square test. Forty-two patients were included for a total of 191 proning sessions, median duration of 16 (5-36) hours. Considering all sessions, PaO 2 /FiO 2 increased (180 [148-210] vs 107 [90-129] mmHg, p < 0.001) and Aa-gradient decreased (127 [92-176] vs 275 [211-334] mmHg, p < 0.001) with proning. C RS (36.2 [30.0-41.8] vs 32.2 [27.5-40.9] ml/cmH 2 O, p = 0.003), VR (2.4 [2.0-2.9] vs 2.3 [1.9-2.8], p = 0.028) and V D /V T HB (0.72 [0.67-0.76] vs 0.71 [0.65-0.76], p = 0.022) slightly increased. Considering the first proning session, PaO 2 /FiO 2 increased (186 [165-215] vs 104 [94-126] mmHg, p < 0.001) and Aa-gradient decreased (121 [89-160] vs 276 [238-321] mmHg, p < 0.001), while C RS , VR and V D /V T HB were unchanged. Similar variations were observed during the subsequent proning sessions. Among the patients who experienced treatment failure (defined as ICU death or need for extracorporeal membrane oxygenation), fewer expressed a positive response in terms of oxygenation (defined as increase of more than 20% in PaO 2 /FiO 2 ) to the first proning (67 vs 97%, p = 0.020). Proning in COVID-19 ARDS intubated patients led to an increase in PaO 2 /FiO 2 and a decrease in Aa-gradient if we consider all the sessions together, the first one or the 4 subsequent sessions independently. When considering all sessions, C RS increased and VR and V D /V T HB only slightly increased.

Published
2022

20. Pulmonary complications associated with veno-arterial extra-corporeal membrane oxygenation: a comprehensive review

Author

Roumy, A., Liaudet, L., Rusca, M., Marcucci, C., and Kirsch, M.

Subjects
surgical procedures, operative, Cardiogenic shock, Extracorporeal membrane oxygenation, Lung injury
Abstract

Veno-arterial extracorporeal membrane oxygenation (VA-ECMO) is a life-saving technology that provides transient respiratory and circulatory support for patients with profound cardiogenic shock or refractory cardiac arrest. Among its potential complications, VA-ECMO may adversely affect lung function through various pathophysiological mechanisms. The interaction of blood components with the biomaterials of the extracorporeal membrane elicits a systemic inflammatory response which may increase pulmonary vascular permeability and promote the sequestration of polymorphonuclear neutrophils within the lung parenchyma. Also, VA-ECMO increases the afterload of the left ventricle (LV) through reverse flow within the thoracic aorta, resulting in increased LV filling pressure and pulmonary congestion. Furthermore, VA-ECMO may result in long-standing pulmonary hypoxia, due to partial shunting of the pulmonary circulation and to reduced pulsatile blood flow within the bronchial circulation. Ultimately, these different abnormalities may result in a state of persisting lung inflammation and fibrotic changes with concomitant functional impairment, which may compromise weaning from VA-ECMO and could possibly result in long-term lung dysfunction. This review presents the mechanisms of lung damage and dysfunction under VA-ECMO and discusses potential strategies to prevent and treat such alterations.

Published
2020

23. Inosine reduces inflammation and improves survival in a murine model of colitis

Author

Mabley, J.G., Pacher, P., Liaudet, L., Soriano, F.G., Hasko, G., Marton, A., Szabo, C., and Salzman, A.L.

Subjects
Adenosine -- Physiological aspects, Colitis -- Care and treatment, Biological sciences
Abstract

Inosine, a naturally occurring purine formed from the breakdown of adenosine, has recently been shown to exert powerful anti-inflammatory effects both in vivo and in vitro. This study evaluated inosine as a potential therapy for colitis. Colitis was induced in mice by the administration of dextran sulfate sodium (DSS). Oral treatment with inosine was begun either before the onset of colitis or as a posttreatment once colitis was established. Evaluation of colon damage and inflammation was determined grossly (body wt, rectal bleeding), histologically, and biochemically (colon levels of MPO, MDA, and cytokines). DSS-induced colitis significantly increased inflammatory cell infiltration into the colon. DSS-induced colitis also increased colon levels of lipid peroxidation, cytokines, and chemokines. Inosine protected the colon from DSS-induced inflammatory cell infiltration and lipid peroxidation. Inosine also partially reduced these parameters in an experimental model of established colitis. Thus inosine treatment may be a potential therapy in colitis. colon; dextran sodium sulfate; cytokines; purine

Published
2003

34. Free Papers

Author

Emmanuel, G., Carranza, S., Vettichira, S., Paradis, M., Lie, T., Kessler, P., Schini-Kerth, V. B., Koh, Y., Hybertson, B. M., Jepson, E. K., Kim, M. J., Lee, I., Lim, C. M., Lee, S. D., Kim, W. S., Kim, D. S., Kim, W. D., Repine, J. E., Takeda, T., Yukioka, T., Matsuda, H., Shimazaki, S., Kammermeier, D., Birkmann, J., Blinzler, L., Gallmeier, W. M., Heuser, D., Jourdain, M., Mangalaboyi, J., Carrette, O., Toumoys, A., Fourrier, F., Mizon, J., Chopin, C., Peake, S. L., Carter, J. K., Russ, R. G., Pierides, J., Leppard, J. P., Porter, K., Galley, H. F., Webster, N. R., Wigmore, S. J., Walsh, T. S., Hopton, P., Lee, A., Ross, J. A., Majcherczyk, P. A., Pugin, J., Glauser, M. P., Heumann, D., Zanetti, G., de Werra, I., Sablotzki, A., Welters, I., Menges, T., Görlach, G., Lehmann, N., Hempelmann, G., Giannitsis, E., Tettenborn, I., Stierle, U., Dalhoff, K., Sheikhzadeh, A., Diederich, K. W., Gant, V., Maciver, C., Treacher, D. F., Lamy, M., Thijs, L. G., Eisele, B., Keinecke, H. -O., Schuster, H. P., Matthias, F. R., Oettinger, W., Hartenauer, U., Fourrier, F., Delvos, U., Stott, S. A., Noble, D. W., Schobersberger, W., Hoffmann, G., Fandrey, J., Bellingan, G. J., Caldwell, H., Dransfield, I., Howie, S. M., Haslett, C., Liaudet, L., Feihl, F., Markert, M., Perret, C., Williams, M. A., Rhoades, C., White, S. A., Miller, J., Withington, S., Newland, A. C., Kelsey, S. M., Froon, A., Bonten, M., Gaillard, C., Greve, J., de Leeuw, P., Drent, M., Stobberingh, E., Buurman, W., Fourcade, O., Simon, M. -F., Leballe, F., Ashraf, R., Sarda, L., Cathala, B., Chap, H., Reper, P., Danckaert, R., Jeunen, R., Bruyns, T., De Hemptinne, J., and Vanderkelen, A.

Published
1996
Full Text
View/download PDF

38. The three biological gaps and hyperoxaluria in ethylene glycol poisoning: case presentation and review.

Author

AHMAD, Y., KISSLING, S., TORRENT, C., CHICHE, J.-D., LIAUDET, L., and LTAIEF, Z.

Abstract

Ethylene glycol is a toxic alcohol which may induce significant toxicity when ingested accidentally or intentionally. The main clinical complications of EG poisoning include central nervous system depression, cardiorespiratory instability and renal failure, which may be lethal if improperly treated. Although the demonstration of high plasma levels of ethylene glycol confirms the intoxication, such measurements are generally not obtained in the acute setting and can be misleading due to the rapid metabolism of EG. This implies the need for alternative, indirect, diagnostic methods, which reflect the metabolic fate of EG. These include an early and transient osmolar gap, followed by an anion gap metabolic acidosis and hyperoxaluria. Another frequent finding is a lactate gap between various methods of lactate measurements. An appropriate knowledge of these laboratory findings is essential for the diagnosis of EG poisoning, and for the initiation of antidote therapy (fomepizole) and hemodialysis in selected cases. These features are illustrated by the presentation of a prototypical case of EG poisoning, in which an incomplete diagnostic workup on hospital admission resulted in an unnecessary laparotomy and a significant delay in the management of the intoxication. [ABSTRACT FROM AUTHOR]

Published
2021

39. A pragmatic approach to the use of inotropes for the management of acute and advanced heart failure: An expert panel consensus

Author

Farmakis, D. Agostoni, P. Baholli, L. Bautin, A. Comin-Colet, J. Crespo-Leiro, M.G. Fedele, F. García-Pinilla, J.M. Giannakoulas, G. Grigioni, F. Gruchała, M. Gustafsson, F. Harjola, V.-P. Hasin, T. Herpain, A. Iliodromitis, E.K. Karason, K. Kivikko, M. Liaudet, L. Ljubas-Maček, J. Marini, M. Masip, J. Mebazaa, A. Nikolaou, M. Ostadal, P. Põder, P. Pollesello, P. Polyzogopoulou, E. Pölzl, G. Tschope, C. Varpula, M. von Lewinski, D. Vrtovec, B. Yilmaz, M.B. Zima, E. Parissis, J.

Abstract

Inotropes aim at increasing cardiac output by enhancing cardiac contractility. They constitute the third pharmacological pillar in the treatment of patients with decompensated heart failure, the other two being diuretics and vasodilators. Three classes of parenterally administered inotropes are currently indicated for decompensated heart failure, (i) the beta adrenergic agonists, including dopamine and dobutamine and also the catecholamines epinephrine and norepinephrine, (ii) the phosphodiesterase III inhibitor milrinone and (iii) the calcium sensitizer levosimendan. These three families of drugs share some pharmacologic traits, but differ profoundly in many of their pleiotropic effects. Identifying the patients in need of inotropic support and selecting the proper inotrope in each case remain challenging. The present consensus, derived by a panel meeting of experts from 21 countries, aims at addressing this very issue in the setting of both acute and advanced heart failure. © 2019 The Authors

Published
2019

40. Free Papers

Author

Sielenkämper, A., Martin, C. M., Madorin, S., Chin-Yee, I., Sibbald, W. J., Ruckoldt, H., Marx, G., Rickels, E., Burchert, W., Vangerow, B., Piepenbrock, S., Kiefer, P., Kosonen, P., Takala, J., Bouachour, G., Richonune, P., Rousselet, M. C., Lemarie, C., Lejeune, G, J. J., Alquier, P., Scheeren, T. W. L., Schwarte, L. A., Fournell, A., Reah, G., Mallick, A., Bodenham, A. R., Przybelski, R., van Iterson, M., Sinaasappel, M., Trouwborst, A., Ince, C., Temmesfeld, B., Mayer, K., Friedland, A., Reich, M., Seeger, W., Grimminger, F., Schwarz, B., Germann, R., Hasibeder, W., Gruber, E., Meusburger, S., Deusch, E., Salak, N., Bonatti, J., Riedmann, B., Rosser, D. M., Stidwill, R. P., Singer, M., Revelly, J. P., Liaudet, L., Frascarolo, Ph., Joseph, J. M., Martinet, O., Markert, M., Madorin, W. S., and Potter, R. F.

Published
1996
Full Text
View/download PDF

44. Free Papers

Author

Kermarrec, N., Karim, A., Beloucif, S., Payen, D., Waurick, R., Booke, M., Bone, H. G., Meyer, J., Prien, Th., Van Aken, H., Datta, P., Magder, S., Rosselet, A., Liaudet, L., Markert, M., Perret, C., Feihl, F., Preiser, J. C., De Backer, D., Debelle, F., Vray, B., Kahn, R. J., and Vincent, J. L.

Published
1996
Full Text
View/download PDF

47. P619Role of Toll-like receptor 5 in the development of post-myocardial infarction inflammation

Author

Parapanov, R., Lugrin, J., Rosenblatt-Velin, N., Waeber, B., Feihl, F., Liaudet, L., Parapanov, R., Lugrin, J., Rosenblatt-Velin, N., Waeber, B., Feihl, F., and Liaudet, L.

Abstract

Background: Inflammatory processes play a key role in the pathophysiology of myocardial infarction (MI). Genetic deletion of toll-like recpetors (TLRs), especially TLR2 and TLR4 have shown protective role in murine models of MI. The role of other TLRs remains unknown. We have previously shown that cardiomyocytes express TLR5 and that the ligand of TLR5, flagellin, activates the NF-kappaB and MAPK pathways in cardiomyocytes. We also have shown that injection of flagellin induces acute systolic dysfunction in vivo in mice. Aim: Determine the role of TLR5 in the development of post-MI inflammation. Methods: A murine model of myocardial infarction was done by a 30 minutes ligation of the left anterior descending coronary artery followed by 2 hours of reperfusion. Infarct size was measured by standard Evans blue/TTC staining. Plasma creatine kinase (CK) was quantified as a read out of myocardial necrosis. Tissue and plasma cytokines (MIP-2, MCP-1, IL-6) were quantified by ELISA. To determine the extent of tissue lipid peroxidation we used malondialdehyde and 4-hydroxynonenal-HIS adduct assays. Tissue protein oxidation was tested by protein carbonyl ELISA kit. Phosphorylation of MAPK was analyzed by western blot. Results: Genetic suppression of TLR5 induced a significant increase of myocardial infarct size and plasma CK, of biochemical markers of myocardial oxidative stress, and cytokine levels in the heart and the plasma after MI. These effects were associated with a marked enhancement of p38 phosphorylation in the heart from TLR5 KO mice. Conclusion: TLR5 protects from acute myocardial injury and reduces local and systemic inflammation during myocardial infarction. The mechanisms may involve reduced p38 signaling, decreased oxidative stress and attenuated cytokine expression. Research supported by the Swiss National Science Foundation, Grant n° 310030_135394/1

Published
2017

48. P90Necrotic cardiomyocytes release soluble pro-inflammatory molecule(s) inducing il1r/myd88-dependent inflammatory responses in cardiac fibroblasts

Author

Lugrin, J., Parapanov, R., Rosenblatt-Velin, N., Waeber, B., Feihl, F., Liaudet, L., Lugrin, J., Parapanov, R., Rosenblatt-Velin, N., Waeber, B., Feihl, F., and Liaudet, L.

Abstract

Background: Inflammation comes out to be a critical biological process in the pathophysiology of myocardial infarction (MI). We hypothesize that this inflammation is triggered by necrotic cardiomyocytes (Cmc) that release a set of endogenous molecules (DAMPs: danger-associated molecular patterns) activating inflammatory responses in cardiac fibroblasts. Aim: Analyze in vitro the immune activation of cardiac fibroblasts exposed to necrotic Cmc conditioned media. Methods: Primary neonatal murine cardiac fibroblasts and Cmc were obtained by digestion of neonatal hearts and differential plating technique allowing a selection for cardiomyocytes and cardiac fibroblasts. Cmc were killed by necrotic stimuli including oxidants (hydrogen peroxide) and mechanic stresses (freeze-thaw). Necrosis was assessed using Hoechst/PI stainings. Fibroblasts were exposed to necrotic Cmc conditioned media and mRNA expression of inflammatory genes was measured by real-time PCR and ELISA. Activation of signaling pathways was analyzed by western blot. We used cardiac cells from Myd88-/-, Trif-/- and Nlrp3-/- animals to evaluate the contribution of TLRs/IL1-R and NLRP3 inflammasome in the sensing of necrotic DAMPs. Results: mRNA expression of chemokines such as MCP-1, MIP-2 and IP-10 were induced in fibroblasts exposed to necrotic Cmc conditioned media. Alternatively, fibroblasts exposed to necrotic fibroblasts conditioned media showed a lower increase in mRNA expression of these chemokines. In addition, in fibroblasts from Myd88-/- mice, response to Cmc conditioned media was fully abrogated whereas no difference was observed in Trif-/- and Nlrp3-/- fibroblasts. Conclusion: Cardiac fibroblasts are able to produce a rapid and specific inflammatory response to necrotic Cmc conditioned media involving the expression of neutrophil and monocyte chemoattractants. The dependence on MyD88 adaptor protein strongly suggests that this response relies on TLR/IL-1R signaling. These results engage cardiac fi

Published
2017

Catalog

Books, media, physical & digital resources
See catalog results