Rassemblement 5. Pharmacologie cardio-vasculaire (60-72)
BETA-BLOCKER TREATMENT IN EXPERIMENTAL HEART FAILURE IN RATS
P. Mansuy, N. Mougenot, J. F Ramirez-Gil, F. Moreau-Raillecove, D. Rousselot-Bonnefond, M. Komajda, Ph. Lechat.
Tutelle de pharmacologie, Conscience Claude Bernard, IFR IPGC, CHU Camaraderie Salpétrière, 47 bd de l’Hôpital, 75013 Paris.
Mechanisms of beneficial effects of beta-blocker treatment in heart failure (HF) in human remain unclear and based on the antagonism of the potential deleterious effects of catecholamines. Since oxydative soucieux is increased in HF, and can be induced by catecholamines, division of the beneficial effect of beta-blockers could be related to a reduction of oxydative soucieux through a reduction of catecholamine release from sympathetic nerve endings. We then tested efficacy of a non selective beta-blocker, propranolol (P) on the experimental model of HF induced in the rat by myocardial infarction secondary to coronary ligation. Three groups of animals were compared: Non infarcted sham (S. n=32), infarcted controls (C, n=30) and propranolol (P) treated animals (45 mg/kg/day, n= 19). P was administrated in drinking water and started six weeks after surgery and given during a six to eight week period. At the time of cessation, a sample of non infarcted myocardium (constitutionnel area) was removed for tordu evaluation of lipidic peroxydation (TBARS determination). Results: Compared to sham animals, hemodynamic parameters were moderately but significantly impaired in infarcted animals and to a similar extend in both groups. Cardiac remodelling was present in infarcted hearts with left ventricular institution and hypertrophy: Left ventricular V.T.T. sectional area (cm2, mean ± sem) was 0.07 ± 0.01 (S), 0.14 ± 0.01 (C), and 0.08 ± 0.007 (P), p