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Protective effects of propranolol on isoproterenol-induced myocardial infarction in arteriosclerotic and non-arteriosclerotic rats

1973; Elsevier BV; Volume: 18; Issue: 1 Linguagem: Inglês

10.1016/0021-9150(73)90114-7

1879-1484

Bernard C. Wexler,

Antibiotics Pharmacokinetics and Efficacy

Arteriosclerotic and non-arteriosclerotic rats were given two s.c. injections of the beta-adrenergic stimulating agent, isoproterenol, (25 and 50 mg/100 g.b.w. respectively) to induce equally massive myocardial infarction. Sub-groups of animals were given the beta-adrenergic blocking agent, propranolol (1.0 mg/100 g b.w., s.c.), three hours prior to isoproterenol. Animals were sacrificed at select time intervals during the acute cardiac necrosis phase and repair phase. Animals pre-treated with propranolol manifested significantly less cardiac necrosis, less excursion of serum GOT, GPT, LDH, glucose, triglycerides, free fatty acids, total cholesterol and corticosterone than isoproterenol-treated animals which showed massive myocardial necrosis, congestive heart failure and marked increase of their serum enzymes, lipids, glucose and corticosterone. The propranolol-treated subjects showed unusual increases in BUN during active cardiac necrosis and persistent hydrothorax during myocardial repair. Histopathologic analyses confirmed the absence of necrosis in propranolol-treated rats but the presence of marked fibroplasia, more severe beta-cell degranulation in isoproterenol-treated subjects and adrenocortical hyperplasia and lipid depletion of the zona glomerulosa commensurate with the severity of congestive heart failure. Arteriosclerotic animals withstood the stress of myocardial infarction better than and responded equally as well as non-arteriosclerotic animals to the necrosis-protecting effects of propranolol.