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16 results on '"Henry, Jean"'

1. Selective Stimulation of Cardiac Lymphangiogenesis Reduces Myocardial Edema and Fibrosis Leading to Improved Cardiac Function Following Myocardial Infarction

Author

Henri, Orianne, primary, Pouehe, Chris, additional, Houssari, Mahmoud, additional, Galas, Ludovic, additional, Nicol, Lionel, additional, Edwards-Lévy, Florence, additional, Henry, Jean-Paul, additional, Dumesnil, Anais, additional, Boukhalfa, Inès, additional, Banquet, Sébastien, additional, Schapman, Damien, additional, Thuillez, Christian, additional, Richard, Vincent, additional, Mulder, Paul, additional, and Brakenhielm, Ebba, additional

Published
2016
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3. Abstract 12624: Therapeutic Lymphangiogenesis Improves Diastolic Function by Limiting Cardiac Edema and Fibrosis After Myocardial Infarction

Author

Henri, Orianne, primary, Houssari, Mahmoud, additional, Pouehe, Chris, additional, Galas, Ludovic, additional, Nicol, Lionel, additional, Edwards-Lévy, Florence, additional, Henry, Jean-Paul, additional, Dumesnil, Anais, additional, Schapman, Damien, additional, Thuillez, Christian, additional, Richard, Vincent, additional, Mulder, Paul, additional, and Brakenhielm, Ebba, additional

Published
2015
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4. Arteriogenic Therapy by Intramyocardial Sustained Delivery of a Novel Growth Factor Combination Prevents Chronic Heart Failure

Author

Banquet, Sébastien, primary, Gomez, Elodie, additional, Nicol, Lionel, additional, Edwards-Lévy, Florence, additional, Henry, Jean-Paul, additional, Cao, Renhai, additional, Schapman, Damien, additional, Dautreaux, Brigitte, additional, Lallemand, Francoise, additional, Bauer, Fabrice, additional, Cao, Yihai, additional, Thuillez, Christian, additional, Mulder, Paul, additional, Richard, Vincent, additional, and Brakenhielm, Ebba, additional

Published
2011
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5. Abstract 3552: Pharmacological Inhibition or Genetic Disruption of Protein Tyrosine Phosphatase 1B Attenuates both Myocardial and Endothelial Dysfunction in Mice with Heart Failure

Author

Vercauteren, Magali, primary, Kurtz, Baptiste, additional, Gomez, Elodie, additional, Henry, Jean-Paul, additional, Bauer, Fabrice, additional, Hooft, Rob, additional, Tremblay, Michel L, additional, Thuillez, Christian, additional, and Richard, Vincent, additional

Published
2008
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6. Response to Letter Regarding Article, “Improvement of Peripheral Endothelial Dysfunction by Protein Tyrosine Phosphatase Inhibitors in Heart Failure”

Author

Vercauteren, Magali, primary, Remy, Elise, additional, Devaux, Corinne, additional, Dautreaux, Brigitte, additional, Henry, Jean-Paul, additional, Bauer, Fabrice, additional, Mulder, Paul, additional, Thuillez, Christian, additional, Richard, Vincent, additional, Hooft van Huijsduijnen, Rob, additional, and Bombrun, Agnès, additional

Published
2007
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7. Improvement of Peripheral Endothelial Dysfunction by Protein Tyrosine Phosphatase Inhibitors in Heart Failure

Author

Vercauteren, Magali, primary, Remy, Elise, additional, Devaux, Corinne, additional, Dautreaux, Brigitte, additional, Henry, Jean-Paul, additional, Bauer, Fabrice, additional, Mulder, Paul, additional, Hooft van Huijsduijnen, Rob, additional, Bombrun, Agnès, additional, Thuillez, Christian, additional, and Richard, Vincent, additional

Published
2006
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8. Long-Term Heart Rate Reduction Induced by the Selective I f Current Inhibitor Ivabradine Improves Left Ventricular Function and Intrinsic Myocardial Structure in Congestive Heart Failure

Author

Mulder, Paul, primary, Barbier, Stephane, additional, Chagraoui, Abdeslam, additional, Richard, Vincent, additional, Henry, Jean Paul, additional, Lallemand, Françoise, additional, Renet, Sylvanie, additional, Lerebours, Guy, additional, Mahlberg-Gaudin, Florence, additional, and Thuillez, Christian, additional

Published
2004
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14. Role of Endogenous Endothelin in Chronic Heart Failure

Author

Mulder, Paul, primary, Richard, Vincent, additional, Derumeaux, Geneviève, additional, Hogie, Manuela, additional, Henry, Jean Paul, additional, Lallemand, Françoise, additional, Compagnon, Patricia, additional, Macé, Bertrand, additional, Comoy, Etienne, additional, Letac, Brice, additional, and Thuillez, Christian, additional

Published
1997
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16. Long-term heart rate reduction induced by the selective I(f) current inhibitor ivabradine improves left ventricular function and intrinsic myocardial structure in congestive heart failure.

Author

Mulder P, Barbier S, Chagraoui A, Richard V, Henry JP, Lallemand F, Renet S, Lerebours G, Mahlberg-Gaudin F, and Thuillez C

Subjects
Animals, Benzazepines therapeutic use, Capillaries drug effects, Cardiac Output drug effects, Collagen analysis, Drug Evaluation, Preclinical, Heart Failure etiology, Heart Failure pathology, Heart Failure physiopathology, Heart Ventricles drug effects, Heart Ventricles pathology, Ion Transport drug effects, Ivabradine, Male, Myocardial Infarction complications, Myocardium chemistry, Rats, Rats, Wistar, Sinoatrial Node drug effects, Stroke Volume drug effects, Ventricular Remodeling drug effects, Benzazepines pharmacology, Heart Failure drug therapy, Heart Rate drug effects, Ventricular Function, Left drug effects
Abstract

Background: Heart rate reduction (HRR) improves left ventricular (LV) filling, increases myocardial O2 supply, and reduces myocardial O2 consumption, which are all beneficial in congestive heart failure (CHF). However, the long-term effects of HRR on cardiac function and remodeling are unknown., Methods and Results: We assessed, in rats with CHF, the effects of long-term HRR induced by the selective I(f) current inhibitor ivabradine (as food admix for 90 days starting 7 days after coronary artery ligation). To assess intrinsic modifications of LV tissue induced by long-term HRR, all parameters were reassessed 3 days after interruption of treatment. Ivabradine decreased heart rate over the 90-day treatment period (-18% versus untreated at 10 mg x kg(-1) x d(-1)), without modifying blood pressure, LV end-diastolic pressure, or dP/dt(max/min). Ivabradine significantly reduced LV end-systolic but not end-diastolic diameter, which resulted in preserved cardiac output due to increased stroke volume. In the Langendorff preparation, ivabradine shifted LV systolic but not end-diastolic pressure-volume relations to the left. Ivabradine decreased LV collagen density and increased LV capillary density without modifying LV weight. Three days after interruption of treatment, the effects of ivabradine on LV geometry, shortening, and stroke volume persisted despite normalization of heart rate., Conclusions: In rats with CHF, long-term HRR induced by the selective I(f) inhibitor ivabradine improves LV function and increases stroke volume, preserving cardiac output despite the HRR. The improvement of cardiac function is related not only to the HRR per se but also to modifications in the extracellular matrix and/or function of myocytes as a consequence of long-term HRR.

Published
2004
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