Vincent Richard

ORCID: 0000-0003-0590-0158
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About
Contact & Profiles
Research Areas
  • Nitric Oxide and Endothelin Effects
  • Cardiac Ischemia and Reperfusion
  • Eicosanoids and Hypertension Pharmacology
  • Cardiovascular Function and Risk Factors
  • Hormonal Regulation and Hypertension
  • Renin-Angiotensin System Studies
  • Cardiac Arrest and Resuscitation
  • Cardiac electrophysiology and arrhythmias
  • Cardiac Imaging and Diagnostics
  • Cardiac Fibrosis and Remodeling
  • Protein Tyrosine Phosphatases
  • Cardiovascular Health and Disease Prevention
  • Systemic Lupus Erythematosus Research
  • Heart Rate Variability and Autonomic Control
  • Cardiovascular, Neuropeptides, and Oxidative Stress Research
  • European and International Law Studies
  • Electron Spin Resonance Studies
  • Pulmonary Hypertension Research and Treatments
  • Anesthesia and Neurotoxicity Research
  • Atherosclerosis and Cardiovascular Diseases
  • European and International Contract Law
  • Apelin-related biomedical research
  • Cardiovascular Disease and Adiposity
  • Heart Failure Treatment and Management
  • Cardiac Valve Diseases and Treatments

Inserm
2015-2024

Université de Rouen Normandie
2015-2024

Centre Hospitalier Universitaire de Rouen
2002-2024

Université Laval
2000-2024

Endothélium, valvulopathies et insuffisance cardiaque
2017-2023

L'Hôpital Nord Franche-Comté
2023

Normandie Université
2013-2022

Université de franche-comté
2016-2022

Centre Hospitalier Universitaire de Besançon
2014-2022

ORCID
2021

Background Experimental evidence suggests that flow-dependent dilatation of conduit arteries is mediated by nitric oxide (NO) and/or prostacyclin. The present study was designed to assess whether NO or prostacyclin also contributes in humans. Methods and Results Radial artery internal diameter (ID) measured continuously 16 healthy volunteers (age, 24±1 years) with a transcutaneous A-mode echo-tracking system coupled Doppler device for the measurement radial blood flow. In 8 subjects,...

10.1161/01.cir.91.5.1314 article EN Circulation 1995-03-01

We have shown previously that preconditioning myocardium with four 5-minute episodes of ischemia and reperfusion dramatically limited the size infarcts caused by a subsequent 40-minute episode sustained ischemia. The current study was undertaken to assess whether same protocol slowed loss high energy phosphates, catabolite accumulation, and/or delayed ultrastructural damage during ischemic episode. Myocardial metabolites ultrastructure in severely subendocardial regions were compared between...

10.1161/01.res.66.4.913 article EN Circulation Research 1990-04-01

Endothelin-1 is an endothelium-derived vasoconstrictor peptide. Its circulating levels are below those known to evoke direct vascular effects. To study whether low concentrations of endothelin-1 potentiate the effects other hormones, we suspended isolated human internal mammary and left anterior descending coronary artery rings in organ chambers for isometric tension recording. In rings, contractions norepinephrine (3 x 10(-8) M) were potentiated by threshold 10(-10) (10(-9) (96 +/- 35% 149...

10.1161/01.cir.82.1.188 article EN Circulation 1990-07-01

Background— The lymphatic system regulates interstitial tissue fluid balance, and malfunction causes edema. heart has an extensive network displaying a dynamic range of lymph flow in physiology. Myocardial edema occurs many cardiovascular diseases, eg, myocardial infarction (MI) chronic failure, suggesting that cardiac transport may be insufficient pathology. Here, we investigate rats the impact MI subsequent failure on network. Further, evaluate for first time functional effects selective...

10.1161/circulationaha.115.020143 article EN Circulation 2016-03-02

Background— Obesity and diabetes mellitus are independently associated with the development of heart failure. In this study, we determined respective effects obesity, insulin resistance, on intrinsic contraction mitochondrial function human myocardium before onset cardiomyopathy. Methods Results— Right atrial was obtained from 141 consecutive patients presenting no sign We investigated ex vivo isometric contraction, respiration calcium retention capacity, respiratory chain complex activities...

10.1161/circulationaha.113.008476 article EN Circulation 2014-06-16

Plasma levels of the vasoconstrictor peptide endothelin (ET) are increased in chronic heart failure (CHF), and ET a major predictor mortality this disease. Thus, may play deleterious role CHF. The purpose study was to assess effects treatment with receptor antagonist bosentan rat model CHF.Rats were subjected coronary artery ligation treated for 2 or 9 months placebo (30 100 mg x kg(-1) d(-1)). Bosentan markedly survival (after months: untreated, 47%; bosentan, 65%; P<.01). Throughout...

10.1161/01.cir.96.6.1976 article EN Circulation 1997-09-16

Heart rate reduction (HRR) improves left ventricular (LV) filling, increases myocardial O2 supply, and reduces consumption, which are all beneficial in congestive heart failure (CHF). However, the long-term effects of HRR on cardiac function remodeling unknown.We assessed, rats with CHF, induced by selective I(f) current inhibitor ivabradine (as food admix for 90 days starting 7 after coronary artery ligation). To assess intrinsic modifications LV tissue HRR, parameters were reassessed 3...

10.1161/01.cir.0000118464.48959.1c article EN Circulation 2004-02-24

Preconditioning myocardium with brief episodes of ischemia reduces energy demand and delays cell death during a subsequent ischemic episode. We hypothesized that postischemic contractile dysfunction after the ("stunning") causes this reduced demand. If hypothesis is correct, then cardioprotection should persist as long mechanical function still depressed at onset sustained ischemia. To analyze temporal relationship between preconditioning stunning, infarct size was compared in two groups...

10.1152/ajpheart.1991.260.3.h796 article EN AJP Heart and Circulatory Physiology 1991-03-01

Repetitive, brief periods of ischemia and reperfusion ("preconditioning") increase the resistance myocardial tissue to subsequent prolonged ischemic episodes limit infarct size. We investigated whether preconditioning also protects against coronary endothelial dysfunction induced by reperfusion.Experiments were performed in four groups rats (n = 8 each group): group 1 underwent sham surgery, 2 subjected 20 minutes left artery occlusion without reperfusion, 3 followed hour 4 (preconditioning...

10.1161/01.cir.89.3.1254 article EN Circulation 1994-03-01

Toll-like receptors (TLR) 2 are expressed in cardiac and inflammatory cells, regulate leukocyte function. Because adhesion is a critical event endothelial injury induced by ischemia/reperfusion (I/R), we assessed whether TLR2 were involved I/R-induced coronary injury.Ischemia-reperfusion markedly decreased NO-mediated relaxations to acetylcholine ex vivo. In contrast, deficient mice, I/R paradoxically improved the responses acetylcholine. To precise cellular compartment expressing which...

10.1161/atvbaha.107.140723 article EN Arteriosclerosis Thrombosis and Vascular Biology 2007-03-02

Microparticles (MPs) are small fragments generated from the plasma membrane after cell stimulation.Among candidate proteins harbored by MPs, we recently showed that sonic hedgehog (Shh) is present in MPs activated/apoptotic human T lymphocytes [Martı ´nez et al., Blood (2006) vol.108, 3012-3020].We show here Shh carried induces nitric oxide (NO) release endothelial cells, triggers changes expression and phosphorylation of enzymes related to NO pathway, decreases production reactive oxygen...

10.1096/fj.07-8079com article EN The FASEB Journal 2007-04-11

Cytochrome-derived epoxyeicosatrienoic acids may be important endothelium-derived hyperpolarizing factors, opening calcium-activated potassium channels, but their involvement in the regulation of arterial stiffness during changes blood flow humans is unknown. In healthy volunteers, we measured pressure, radial artery diameter, wall thickness, and (NIUS02) hand skin heating presence saline or inhibitors NO synthase (N(G)-monomethyl-L-arginine), channels (tetraethylammonium), cytochrome...

10.1161/hypertensionaha.109.142190 article EN Hypertension 2010-01-19

Lymphatics play an essential pathophysiological role in promoting fluid and immune cell tissue clearance. Conversely, cells may influence lymphatic function remodeling. Recently, cardiac lymphangiogenesis has been proposed as a therapeutic target to prevent heart failure after myocardial infarction (MI). We investigated the effects of gene therapy modulate post-MI rodents. Second, we determined impact cardiac-infiltrating T on remodeling heart. Approach Results: Comparing adenoviral versus...

10.1161/atvbaha.120.314370 article EN cc-by-nc-nd Arteriosclerosis Thrombosis and Vascular Biology 2020-05-14

We report here a unique example of an in situ generated aluminum initiator stabilized by C2-symmetric salen ligand which shows hitherto unknown high activity for the ROP rac-lactide at room temperature. Using simple and robust catalyst system, is prepared from complex onium salt, this convenient route employs readily available reagents that afford polylactide good yields with narrow polydispersity indices, without need time-consuming expensive processes are typically required preparation...

10.1021/jacs.7b01749 article EN Journal of the American Chemical Society 2017-04-11

Continuous production of nitric oxide (NO) from endothelial cells permanently inhibits the synthesis and vasoconstrictor effects endothelin. Thus, inhibition NO might unmask a vasopressor response to To assess whether endothelin contributes pressor induced by synthesis, we tested bosentan, nonpeptide antagonist ETA ETB receptors, affected hypertensive synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME).Anesthetized rats received increasing doses L-NAME (0.1 3 mg.kg-1) in absence or...

10.1161/01.cir.91.3.771 article EN Circulation 1995-02-01

BACKGROUND-Chronic heart failure (CHF) impairs the endothelium-dependent, flow-mediated dilation (FMD) of small arteries. However, whether chronic angiotensin-converting enzyme (ACE) inhibition affects impairment FMD in CHF is unknown. We investigated effects long-term ACE on peripheral arteries rats with and mechanism(s) involved. METHODS AND RESULTS-FMD was assessed isolated, perfused gracilis muscle from sham-operated, untreated or inhibitor-treated (perindopril 2 mg. kg(-1). day(-1) for...

10.1161/01.cir.102.3.351 article EN Circulation 2000-07-18

The myocardial velocity gradient (MVG) is a recent index of regional function derived from endocardial and epicardial velocities obtained by tissue Doppler imaging (TDI). This might be useful for discriminating between physiological pathological left ventricular hypertrophy (LVH) documenting the early transition compensated LVH to heart failure. We sought compare MVG measured across posterior wall normal rats with (exercise) (pressure-overload) LVH.Wistar were assigned one following groups:...

10.1161/01.cir.0000012943.91101.d7 article EN Circulation 2002-04-02

Flow-mediated dilatation (FMD) of the peripheral arteries may be impaired in chronic heart failure (CHF), and this could contribute to increased resistance exercise intolerance that occur with disease. Physical improves FMD large conduit CHF, but whether a similar impairment also occurs smaller is unknown. The mechanisms changes after CHF or are unknown.FMD was assessed isolated, perfused, preconstricted gracilis muscle from sham-operated rats (coronary artery ligation) who were either...

10.1161/01.cir.99.22.2951 article EN Circulation 1999-06-08

Recent studies suggest that polymorphonuclear leukocytes (PMNs) may cause additional myocyte injury during reperfusion of ischemic myocardium. The present study was done to investigate whether PMNs accumulate in myocardium early after reversible or irreversible injury. Open-chest anesthetized dogs underwent circumflex coronary occlusions for 12 min (n = 5), 40 8), 90 followed by 1 h reperfusion. Autologous were radiolabeled with 111In and reinjected quantitate myocardial PMN influx reflow....

10.1152/ajpheart.1988.255.5.h1188 article EN AJP Heart and Circulatory Physiology 1988-11-01
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