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9. Vitamin C deficiency exerts paradoxical cardiovascular effects in osteogenic disorder Shionogi (ODS) rats

Author

Vergely, Catherine, Goirand, Francoise, Ecarnot-Laubriet, Aline, Renard, Celine, Moreau, Daniel, Guilland, Jean-Claude, Dumas, Monique, and Rochette, Luc

Subjects
Vitamin C deficiency, Rattus, Rats, Myocardial ischemia, Arrhythmia, Thoracic arteries, Food/cooking/nutrition
Abstract

Vitamin C is considered to be a very efficient water-soluble antioxidant, for which several new cardiovascular properties were recently described. The aim of this study was to determine in vivo the effects of a severe depletion of vitamin C on cardiac and vascular variables and reperfusion arrhythmias. For this purpose, we used a mutant strain of Wistar rats, osteogenic disorder Shionogi (ODS). After 15 d of consuming a vitamin C-deficient diet, ODS rats had a 90% decrease in plasma and tissue levels of ascorbate compared with ODS vitamin C-supplemented rats and normal Wistar rats. However, plasma antioxidant capacity, proteins, [alpha]-tocopherol, urate, catecholamines, lipids, and nitrate were not influenced by the vitamin C deficiency in ODS rats. Moreover, there was no difference between ODS vitamin C-deficient and -supplemented rats in heart rate and arterial pressure. After 5 min of an in vivo regional myocardial ischemia, various severe arrhythmias were observed, but their intensities were not modified by vitamin C in vitamin C-deficient ODS rats, The vascular reactivity, measured in vitro on thoracic arteries, was not altered by ascorbate deficiency in ODS rats. These unexpected results suggest that unidentified compensatory mechanisms play a role in maintaining normal cardiac function and vascular reactivity in vitamin C-deficient rats. KEY WORDS: * ascorbic acid * myocardial ischemia-reperfusion * arrhythmia * oxidative stress * ODS rats

Published
2004

15. Sufficient levels of quinine in the serum circumvent the multidrug resistance of the human leukemic cell line K562/ADM

Author

Solary, Eric, Velay, Isabelle, Chauffert, Bruno, Bidan, Jeanne-Marie, Caillot, Denis, Dumas, Monique, and Guy, Henri

Subjects
Quinine -- Health aspects, Antineoplastic agents -- Physiological aspects, Drug resistance -- Drug therapy, Chemotherapy, Combination -- Complications, Health
Abstract

Unfortunately, cancer cells sometimes develop resistance to the toxic effects of anticancer drugs. Drug resistance can develop by several different mechanisms. One mechanism results in the simultaneous development of resistance to several drugs and is appropriately called multidrug resistance (MDR). Often patients with acute leukemia or multiple myeloma respond favorably to chemotherapy only to relapse and die because cancer cells have become unresponsive to chemotherapeutic agents. Multidrug resistance seems to result from the expression of a protein in the cancer cell membrane; this protein acts as a pump and pushes many types of chemotherapeutic agents back out of the cancer cell. Insufficient amounts of drug accumulate within the cell, and the cancer cell escapes the toxic effects of treatment. This phenomenon can be studied in vitro, that is, in cells grown under laboratory conditions. Researchers have identified many substances that can block this pumping action, and in principle, render the cancer cells once again susceptible to chemotherapy. However, the amounts of the substances used in the laboratory could never be used inside the human body. More recently, researchers found that the drug quinine, famous as one of the first effective treatments for malaria, may block multidrug resistance. More importantly, quinine appears to block MDR at concentrations practical for medical treatment. An experimental treatment protocol including quinine has begun for patients with leukemia or multiple myeloma refractory (resistant) to treatment. Using cultures of the experimental human leukemic cell designated K562/ADM, researchers found that blood samples taken from the patients contained sufficient quinine to block the MDR in laboratory experiments. This demonstrates that the amount of quinine in the blood of human cancer patients can be sufficient to block multidrug resistance in leukemic cells. However, it remains to be determined if this effect observed in laboratory dishes will affect the leukemic cells in patients' bodies in the same manner. (Consumer Summary produced by Reliance Medical Information, Inc.)

Published
1991

21. ADRB3 adrenergic receptor is a key regulator of human myometrial apoptosis and inflammation during chorioamnionitis

Author

Lirussi, Fréderic, Rakotoniaina, Zo, Madani, Siham, Goirand, Françoise, Breuiller-Fouché, Michelle, Leroy, Marie-Josèphe, Sagot, Paul, Morrison, John, Dumas, Monique, Bardou, Marc, Laboratoire de Pharmacologie et Toxicologie, Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), La grossesse normale et pathologique: développement et fonctions du placenta et de l'utérus (UMR_S 767), Institut des sciences du Médicament -Toxicologie - Chimie - Environnement (IFR71), Institut National de la Santé et de la Recherche Médicale (INSERM)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Paris Descartes - Paris 5 (UPD5)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Departments of Gynaecology and Obstetrics, Clinical Science Institute-National University of Ireland [Galway] (NUI Galway), Hôpital du Bocage, Centre d'Investigation Clinique 1432 (Dijon) - Module Plurithématique : Périnatalité Cancérologie Handicap et Ophtalmologie (CIC-P803), Université de Bourgogne (UB)-Direction Générale de l'Organisation des Soins (DGOS)-Institut National de la Santé et de la Recherche Médicale (INSERM), Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand ( CHU Dijon ), La grossesse normale et pathologique: développement et fonctions du placenta et de l'utérus ( UMR_S 767 ), Institut des sciences du Médicament -Toxicologie - Chimie - Environnement ( IFR71 ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL ( ENSCP ) -Centre National de la Recherche Scientifique ( CNRS ) -Institut de Recherche pour le Développement ( IRD ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL ( ENSCP ) -Centre National de la Recherche Scientifique ( CNRS ) -Institut de Recherche pour le Développement ( IRD ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Clinical Science Institute-National University of Ireland [Galway] ( NUI Galway ), Unité de Pharmacologie Clinique, Laboratoire de Physiopathologie et de Pharmacologie Cardiovasculaire Expérimentale (LPPCE), Université de Bourgogne (UB), Institut de Recherche pour le Développement (IRD)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Service de Gynécologie Obstétrique, Médecine Foetale et Stérilité Conjugale - Chirurgie Gynécologie et Oncologique [CHU de Dijon], and Breuiller-Fouche, Michelle

Subjects
Lipopolysaccharides, MESH : Benzoates, MESH: Inflammation, Pregnancy Trimester, Third, MESH : Cytokines, MESH : Receptors, Adrenergic, beta-3, MESH: Sulfonamides, Adrenergic beta-3 Receptor Agonists, Apoptosis, MESH : Pregnancy Trimester, Third, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, MESH : Lipopolysaccharides, Benzoates, MESH : Chorioamnionitis, MESH: Pregnancy, Pregnancy, Humans, MESH : Female, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, MESH : Sulfonamides, Inflammation, Sulfonamides, MESH: Cytokines, MESH : Inflammation, MESH: Humans, [ SDV.BC ] Life Sciences [q-bio]/Cellular Biology, MESH : Myometrium, MESH: Apoptosis, MESH: Chorioamnionitis, MESH : Humans, MESH: Benzoates, MESH : Pregnancy, Chorioamnionitis, Receptors, Adrenergic, beta-3, Myometrium, MESH: Pregnancy Trimester, Third, Cytokines, MESH: Myometrium, Female, MESH: Lipopolysaccharides, MESH: Receptors, Adrenergic, beta-3, MESH: Female, MESH : Apoptosis
Abstract

International audience; The pathophysiology underlying preterm labor triggered by inflammatory conditions such as chorioamnionitis remains largely unclear. It has already been suggested that beta-3 adrenergic (ADRB3) agonists might be of interest in the pharmacological management of preterm labor. Although there is evidence implicating ADRB receptors in the control of inflammation, there are minimal data relating specifically to ADRB3. To explore the cellular consequences of chorioamnionitis and detect apoptosis, we first performed immunostaining and Western blot experiments on human myometrial samples obtained from women with confirmed chorioamnionitis. We then developed an in vitro model of chorioamnionitis by incubating the myometrial samples obtained from uncomplicated pregnancies with Escherichia coli lipopolysaccharide (LPS). We observed that chorioamnionitis was associated with a significant increase in cleaved CASP3 protein expression, as well as chromatin condensation, which were reproduced experimentally by LPS stimulation (10 microg/ml, 48 h). Lipopolysaccharide stimulation of normal human myometrium also induced CASP3 transcripts, increased the proapoptotic marker BAX, and decreased the antiapoptotic marker BCL2. Lipopolysaccharide-induced apoptosis was antagonized by neutralization of secreted tumor necrosis factor by a specific antibody. Furthermore, LPS stimulation increased medium culture levels of proinflammatory cytokines interleukin 6 (IL6) and IL8. Lipopolysaccharide-induced apoptosis and cytokine production were prevented by the new and potent ADRB3 agonist SAR150640 in a concentration-dependent manner. SAR150640 by itself did not exhibit any effect on apoptosis or cytokine production in control tissues. This study shows that chorioamnionitis is associated with apoptosis of human myometrial cells. It emphasizes the potential therapeutic interest of ADRB3 agonists in the field of preterm labor and other inflammatory conditions.

Published
2008
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22. Stimulation of the ADRB3 adrenergic receptor induces relaxation of human placental arteries: influence of preeclampsia

Author

Rouget, Céline, Barthez, O., Goirand, Françoise, Leroy, Marie-Josèphe, Breuiller-Fouché, Michelle, Rakotoniaina, Zo, Guérard, P., Morcillo, Esteban, Advenier, C., Sagot, Paul, Cabrol, Dominique, Dumas, Monique, Bardou, Marc, Laboratoire de Physiopathologie et de Pharmacologie Cardiovasculaire Expérimentale ( LPPCE ), Université de Bourgogne ( UB ), Pharmacologie, Université Paris Descartes - Paris 5 ( UPD5 ) -EA220, Développement humain : Croissance et différenciation, Institut des sciences du Médicament -Toxicologie - Chimie - Environnement ( IFR71 ), Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL ( ENSCP ) -Centre National de la Recherche Scientifique ( CNRS ) -Institut de Recherche pour le Développement ( IRD ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ) -Ecole Nationale Supérieure de Chimie de Paris- Chimie ParisTech-PSL ( ENSCP ) -Centre National de la Recherche Scientifique ( CNRS ) -Institut de Recherche pour le Développement ( IRD ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Université Paris Descartes - Paris 5 ( UPD5 ) -Institut National de la Santé et de la Recherche Médicale ( INSERM ), Department of Pharmacology, Universitat de València ( UV ), Maternité, Obstétrique et Gynécologie, Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand ( CHU Dijon ), Maternité Port-Royal [CHU Cochin], CHU Cochin [AP-HP]-Assistance publique - Hôpitaux de Paris (AP-HP), Supported, in part, by the Fondation pour la Recherche Médicale and, in part, by the grant SAF2003–07206-C02 (Spain)., Breuiller-Fouche, Michelle, Laboratoire de Physiopathologie et de Pharmacologie Cardiovasculaire Expérimentale (LPPCE), Université de Bourgogne (UB), Université Paris Descartes - Paris 5 (UPD5)-EA220, Institut des sciences du Médicament -Toxicologie - Chimie - Environnement (IFR71), Institut de Recherche pour le Développement (IRD)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Centre National de la Recherche Scientifique (CNRS)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Universitat de València (UV), Service de Gynécologie Obstétrique, Médecine Foetale et Stérilité Conjugale - Chirurgie Gynécologie et Oncologique [CHU de Dijon], Centre Hospitalier Universitaire de Dijon - Hôpital François Mitterrand (CHU Dijon), Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Hôpital Cochin [AP-HP], Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP), Institut National de la Santé et de la Recherche Médicale (INSERM)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM)-Ecole Nationale Supérieure de Chimie de Paris - Chimie ParisTech-PSL (ENSCP), Université Paris sciences et lettres (PSL)-Université Paris sciences et lettres (PSL)-Centre National de la Recherche Scientifique (CNRS)-Institut de Recherche pour le Développement (IRD)-Université Paris Descartes - Paris 5 (UPD5)-Université Paris Descartes - Paris 5 (UPD5)-Institut National de la Santé et de la Recherche Médicale (INSERM), Hôpital Cochin [AP-HP], and Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)-Assistance publique - Hôpitaux de Paris (AP-HP) (AP-HP)

Subjects
MESH: Pre-Eclampsia, Placenta, MESH : Receptors, Adrenergic, beta-3, MESH : Adrenergic beta-Agonists, MESH : Receptors, Adrenergic, beta-2, MESH : Isoproterenol, MESH: Adrenergic beta-Agonists, MESH: Isoproterenol, MESH : Vasodilation, MESH: Pregnancy, Pre-Eclampsia, Pregnancy, MESH : Female, MESH : Albuterol, MESH : Pre-Eclampsia, Arteries, Adrenergic beta-Agonists, MESH: Placenta, MESH: Tetrahydronaphthalenes, Vasodilation, MESH: Nucleotides, Cyclic, MESH : Placenta, Ethanolamines, MESH : Tetrahydronaphthalenes, Female, Nucleotides, Cyclic, Tetrahydronaphthalenes, Adrenergic beta-3 Receptor Agonists, [SDV.BC]Life Sciences [q-bio]/Cellular Biology, MESH: Ethanolamines, MESH: Vasodilation, MESH : Ethanolamines, Humans, Albuterol, [SDV.BC] Life Sciences [q-bio]/Cellular Biology, MESH: Arteries, Adrenergic beta-2 Receptor Agonists, MESH: Humans, [ SDV.BC ] Life Sciences [q-bio]/Cellular Biology, MESH: Albuterol, MESH : Humans, Isoproterenol, MESH : Arteries, MESH : Nucleotides, Cyclic, MESH : Pregnancy, Receptors, Adrenergic, beta-3, Receptors, Adrenergic, beta-2, MESH: Receptors, Adrenergic, beta-3, MESH: Receptors, Adrenergic, beta-2, MESH: Female
Abstract

International audience; Preeclampsia, which complicates 3-8% of pregnancies, is one of the leading causes of neonatal morbidity and mortality. Its pathophysiology remains unclear. The aim of the present study was to investigate the presence and the role of beta2- and beta2-adrenergic receptors (ADRB2 and ADRB3, respectively) in human placental arteries and to assess the influence of preeclampsia on ADRB responsiveness. SR 59119A, salbutamol, and isoproterenol (ADRB3, ADRB2, and nonselective ADRB agonists, respectively) induced a concentration-dependent relaxation of placental artery rings obtained from women with uncomplicated or preeclamptic pregnancies. SR 59119A-induced relaxation was unaffected by the blockade of ADRB1 and ADRB2 by 0.1 microM propranolol but was significantly decreased by the blockade of ADRB1, ADRB2, and ADRB3 by 10 microM propranolol. Both SR 59119A and salbutamol were associated with a significant increase in cAMP production that was significantly inhibited by pretreatment with 0.1 microM propranolol only for salbutamol. SR 59119A-induced relaxation (E(max) = 28% +/- 5% vs. 45% +/- 4%, respectively) and cAMP production (2.7 +/- 0.5 vs. 4.9 +/- 0.4 pmol/mg of protein, respectively; P < 0.01) were decreased in arteries obtained from preeclamptic compared to normotensive women. Both ADRB2 and ADRB3 transcripts were expressed at the same level between arteries from normotensive and preeclamptic women. Western blot analysis, however, revealed a decreased expression of the ADRB3 immunoreactive protein in arteries from preeclamptic compared to normotensive women. We suggest the presence of functional ADRB2 and ADRB3 in human placental arteries. Even if preeclampsia is associated with an impairment of the ADRB3 responsiveness, ADRB3 agonists may have future pharmaceutical implications in the management of pregnancy-related disorders.

Published
2005
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23. Role of potassium channels and nitric oxide in the relaxant effects elicited by β-adrenoceptor agonists on hypoxic vasoconstriction in the isolated perfused lung of the rat

Author

Dumas, Jean-Paul, Goirand, Françoise, Bardou, Marc, Dumas, Monique, Rochette, Luc, Advenier, Charles, and Giudicelli, Jean-François

Subjects
Male, Pulmonary Circulation, Potassium Channels, Muscle Relaxation, Adrenergic beta-Agonists, In Vitro Techniques, Nitric Oxide, Muscle, Smooth, Vascular, Rats, NG-Nitroarginine Methyl Ester, Vasoconstriction, Papers, Glyburide, Potassium Channel Blockers, Respiratory Mechanics, Animals, Cyclooxygenase Inhibitors, Enzyme Inhibitors, Nitric Oxide Synthase, Rats, Wistar, Hypoxia, Lung
Abstract

1. The aims of this study were to compare, in the rat isolated perfused lung preparation, the antagonist effects of a nonselective beta-adrenoceptor agonist (isoprenaline), a selective beta2-adrenoceptor agonist (salbutamol) and a selective beta3-adrenoceptor agonist (SR 59104A) on the hypoxic pulmonary pressure response, and to investigate the role of K+ channels, endothelium derived relaxing factor and prostaglandins in these effects. K+ channels were inhibited by glibenclamide, charybdotoxin or apamin, NO synthase and cyclo-oxygenase were inhibited by N(G)-nitro-L-arginine methyl ester (L-NAME) and indomethacin, respectively. 2. Hypoxic ventilation produced a significant increase in perfusion pressure (+65%, P0.001) and L-NAME significantly increased this response further (+123%, P0.01). After apamin, L-NAME, indomethacin, post-hypoxic basal pressure did not return to baseline values (P0.001). 3. Glibenclamide partially inhibited the relaxant effects of isoprenaline (P0.05) and salbutamol (P0.001) but not that of SR 59104A. In contrast, charybdotoxin and apamin partially inhibited the relaxant effects of SR 59104A (P=0.053 and0.01, respectively) but did not modify the effects of isoprenaline and salbutamol. L-NAME partially inhibited the dilator response of salbutamol (P0.01) and SR 59104A (P0.05) but not that of isoprenaline. 4. We conclude that (a) EDRF exerts a significant inhibition of the hypoxic pulmonary response, (b) SK(Ca) channel activation, EDRF and prostaglandins contribute to the reversal of the hypoxic pressure response, (c) the vasodilation induced by isoprenaline is mediated in part by activation of K(ATP) channels, that of salbutamol by activation of K(ATP) channels and EDRF. In contrast, SR 59104A partly operates through BK(Ca), SK(Ca), channels and EDRF activation, differing in this from the beta1 and beta2-adrenoceptor agonists.

Published
1999

26. Dose-dependent biphasic leptin-induced proliferation is caused by non-specific IL-6/ NF-κB pathway activation in human myometrial cells.

Author

Barrichon, Marina, Hadi, Tarik, Wendremaire, Maeva, Ptasinski, Clémentine, Seigneuric, Renaud, Marcion, Guillaume, Delignette, Marc, Marchet, Jacques, Dumas, Monique, Sagot, Paul, Bardou, Marc, Garrido, Carmen, and Lirussi, Frédéric

Subjects
INTERLEUKINS, NF-kappa B, SMOOTH muscle, CELL proliferation, LEPTIN receptors, OVERWEIGHT women, PARTURITION, DURATION of pregnancy, DISEASES
Abstract

Background and Purpose Leptin, an adipokine synthesized by the placenta during pregnancy, has been proposed for the management of preterm labour ( PTL), as it is able to prevent in vitro uterine contractility and remodelling associated with labour onset. Another common feature of labour onset is the phenotypic switch of myometrial smooth muscle cells from a proliferative to a hypertrophic state. As proliferative effects have been demonstrated for leptin in other tissues, we aimed to investigate its ability to induce myometrial proliferation and thus to maintain uterine quiescence. Experimental Approach We stimulated human primary myometrial smooth muscle cells with leptin in the presence or absence of receptor antagonists or signalling pathway inhibitors. Key Results Leptin induced myometrial cell proliferation in a biphasic manner. At 6.25 ng·mL−1, leptin-induced proliferation was mediated by the leptin receptor and required the early activation of ERK1/2. At a concentration above 25 ng·mL−1, leptin induced direct non-specific stimulation of the IL-6 receptor, leading to NF-κB activation, and exerted anti-proliferative effects. However, at 50 ng·mL−1, leptin re-induces proliferation via IL-6 receptor stimulation that requires STAT3 and delayed ERK1/2 activation. Conclusions and Implications These data bring new insights into leptin signalling-induced myometrial proliferation and its interrelationship with the IL-6/ IL-6 receptor axis. In the light of our previous work, the present study emphasizes the potential value of leptin in the pharmacological management of PTL and it also strengthens the hypothesis that leptin might be a contributory factor in the parturition-related disorders observed in obese women. [ABSTRACT FROM AUTHOR]

Published
2015
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27. Increased superoxide anion production is associated with early atherosclerosis and cardiovascular dysfunctions in a rabbit model

Author

Collin, Bertrand, primary, Busseuil, David, additional, Zeller, Marianne, additional, Perrin, Caroline, additional, Barthez, Olivier, additional, Duvillard, Laurence, additional, Vergely, Catherine, additional, Bardou, Marc, additional, Dumas, Monique, additional, Cottin, Yves, additional, and Rochette, Luc, additional

Published
2006
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29. Relaxant Effects of Selective Phosphodiesterase Inhibitors on U46619 Precontracted Human Intralobar Pulmonary Arteries and Role of Potassium Channels

Author

Bardou, Marc, primary, Goirand, Françoise, additional, Bernard, Alain, additional, Guerard, Pascal, additional, Gatinet, Mylene, additional, Devillier, Philippe, additional, Dumas, Jean-Paul, additional, Morcillo, Esteban J., additional, Rochette, Luc, additional, and Dumas, Monique, additional

Published
2002
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45. Urinary β2-microglobulin early indicator of high dose cisdiamminedichloroplatinum nephrotoxicity? Influence of furosemide.

Author

Gislain, Catherine, Dumas, Monique, d'Athis, Philippe, Lautissier, Jean-Louis, Escousse, André, and Guerrin, Jacques

Abstract

To evaluate the efficacy of β2-microglobulin as an indicator of cisplatinum nephrotoxicity, creatinine clearance and urinary β2-microglobulin were measured in 19 patients during 5 h after administration of a single dose of 80 mg/m cisplatinum. Eleven patients received furosemide as a concomitant therapy. Serum creatinine and β2-microglobulin remained unchanged. A decrease of creatinine clearance was observed. Urinary β2-microglobulin increased between 1 and 3 h after administration. This suggests transient tubular damage immediately after the treatment course. The concomitant administration of furosemide does not modify these results. However, patients who developped long-term nephrotoxicity had no early rise of urinary β2-microglobulin excretion; thus, it is not possible to predict cumulative nephrotoxicity by measuring β2-microglobulin immediately after the first course of high-dose cisplatinum. [ABSTRACT FROM AUTHOR]

Published
1986
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46. Influence of hydration on ultrafilterable platinum kinetics and kidney function in patients treated with cis-diamminedichloroplatinum(II).

Author

Dumas, Monique, Gislain, Catherine, d'Athis, Philippe, Chadoint-Noudeau, Viviane, Escousse, André, Guerrin, Jacques, Autissier, Nicole, Dumas, M, de Gislain, C, d'Athis, P, Chadoint-Noudeau, V, Escousse, A, Guerrin, J, and Autissier, N

Subjects
BIOTRANSFORMATION (Metabolism), CHLORIDES, CISPLATIN, COMPARATIVE studies, CREATININE, GLUCANS, GLUCOSE, KIDNEYS, RESEARCH methodology, MEDICAL cooperation, PLATINUM, RESEARCH, STATISTICAL sampling, SODIUM, URODYNAMICS, EVALUATION research, RANDOMIZED controlled trials, HYPERTONIC saline solutions
Abstract

It has been reported that hypertonic saline provides protection against the renal toxicity of cisplatin (CDDP). We therefore evaluated its influence on the plasma and urinary pharmacokinetics of ultrafilterable platinum and kidney function as estimated by creatinine, inulin and PAH clearance. We undertook a randomized trial including two groups of ten patients receiving 100 mg/m2 CDDP in isotonic (group 1) or hypertonic saline (group 2) by a 20-min infusion. The hydration consisted of dextrose in group 1 and isotonic saline in group 2. Maximal concentration (Cmax), protein binding and cumulative urinary excretion were significantly higher in the dextrose group. Urinary flow decreased in this group but not in the other one. Inulin clearance was higher in the dextrose group than in the saline group and P-aminohippuric acid (PAH) clearance was not significantly different in these groups of patients. Hyponatremia was observed in the dextrose group. These results suggest that hypertonic saline infusion and saline hydration may enhance the diffusion of CDDP into tissues, lowering Cmax and renal excretion of platinum. The reduction of protein binding may indicate a diminution of aquation of CDDP in plasma. Our results suggest that the infusion of CDDP in hypertonic saline with salt hydration could exert a protective effect on the kidney. Moreover, there is a lessening of the risk of cellular hyperhydration. However, the better influence of dextrose hydration on glomerular filtration leads us to recommend a combination of the two methods of hydration for better tolerance and efficacy. [ABSTRACT FROM AUTHOR]

Published
1990
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48. ETA, Mixed ETA/ETBReceptor Antagonists, and Protein Kinase C Inhibitor Prevent Acute Hypoxic Pulmonary Vasoconstriction Influence of Potassium Channels

Author

Goirand, Françoise, Bardou, Marc, Guerard, Pascal, Dumas, Jean-Paul, Rochette, Luc, and Dumas, Monique

Abstract

The aims of this study were to investigate the effects of a selective ETA(BQ-123), a selective ETB(BQ-788), and a specific mixed ETA/ETBreceptor antagonist (bosentan) on the pulmonary vasoconstriction induced by hypoxia in the isolated perfused rat lung, and the role of nitric oxide, adenosine triphosphate–sensitive (KATP), large conductance Ca-activated (BKCa) and 4-aminopyridine–sensitive voltage-gated Kchannels (KV) in the relaxant effects of the selective ETAreceptor antagonist BQ-123 and a protein kinase C inhibitor, bisindolylmaleimide I. Kchannels were inhibited by glibenclamide, charybdotoxin, and 4-aminopyridine and nitric oxide synthase by l-NG-nitroarginine methyl ester (l-NAME). Hypoxic ventilation produced a significant pressure response (57, p < 0.001). BQ-123, bosentan, and bisindolylmaleimide I induced a concentration-dependent decrease of the hypoxic pressure response (p < 0.001), whereas BQ-788 did not exhibit any inhibitory effect against hypoxic pressure response. Glibenclamide, charybdotoxin, and 4-aminopyridine partially opposed the inhibitory effects elicited by BQ-123 (p < 0.05), but l-NAME did not modify these effects. The effects of bisindolylmaleimide I on hypoxic pressure response were unaffected by glibenclamide, charybdotoxin, or 4-aminopyridine. The authors conclude that (a) ETAreceptors and protein kinase C are involved in the modulation of hypoxic pulmonary vasoconstriction; and (b) the ETAantagonist BQ-123 opposes hypoxic pulmonary vasoconstriction through KATP, Kv, and BKCachannels, differing in this from the protein kinase C inhibitor bisindolylmaleimide I. These results suggest that BQ-123 operates through a mechanism independent of bisindolylmaleimide I–inhibited protein kinase C isoforms.

Published
2003

49. Differential Retention of Doxorubicin in the Organs of Two Strains of Rats

Author

Chauffert, Bruno, Dumas, Monique, Dubuet, Aleth, D'Athis, Philippe, and Olsson, Nils Olivier

Abstract

Fluorescence microscopy and high pressure liquid chromatography were used to study the decrease of doxorubicin (DXR) concentrations in the liver, spleen, heart, lung, kidney and skeletal muscle of two strains of rats at various times after a single intravenous injection of the drug (8 mg kg−1). DXR was located within the cell nucleus and was mostly undegraded, it persisted, especially in heart, lungs and spleen where it was detectable 10 days after injection. The DXR/DNA ratio, was used as an index of nuclear fixation of the drug. A major difference in the DXR/DNA ratio between the two strains were observed in heart and spleen results; the DXR/DNA ratio was significantly higher in heart and spleen compared with lung, liver and kidney in both strains.

Published
1988
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50. Role of potassium channels and nitric oxide in the effects of iloprost and prostaglandin E1on hypoxic vasoconstriction in the isolated perfused lung of the rat

Author

Dumas, Monique, Dumas, Jean‐Paul, Rochette, Luc, Advenier, Charles, and Giudicelli, Jean‐François

Abstract

1The aims of this study were to compare in the rat isolated perfused lung preparation, the antagonist effects of iloprost, a stable analogue of prostacyclin, and prostaglandin E1(PGE1) on the hypoxic pulmonary pressure response, and to investigate the possible involvement of KATPand KCachannels and of EDRF (NO) in these effects. In addition, iloprost and PGE1effects were compared to those of adenosine and forskolin.2Isolated lungs from male Wistar rats (260–320 g) were ventilated with 21% O2+ 5% CO2+ 74% N2(normoxia) or 5% CO2+ 95% N2(hypoxia) and perfused with a salt solution supplemented with ficoll. Glibenclamide (1 μm), charybdotoxin (0.1 μm), NG‐nitro‐L‐arginine methyl ester (l‐NAME, 100 μm) were used to block KATP, KCachannels and NO synthesis, respectively.3Iloprost, PGE1, adenosine and forskolin caused relaxation during the hypoxic pressure response. The order of potency was: iloprost > PGE1= forskolin > adenosine. EC50values were 1.91 ± 0.52 10−9M, 3.31 ± 0.58 10−7M, 3.24 ± 0.78 10−7M and 7.70 ± 1.68 10−5M, respectively. Glibenclamide, charybdotoxin and L‐NAME inhibited partially the relaxant effects of iloprost and forskolin but not those of PGE1.4It is concluded that in the rat isolated lung preparation, iloprost and forskolin but not PGE1dilate pulmonary vessels partly through KATPchannels, KCachannels and nitric oxide release. Furthermore our results suggest that the role of cyclic AMP in these effects is not unequivocal.

Published
1997
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