Male and female, arteriosclerotic and non-arteriosclerotic rats were treated with the anti-lipemic agent,
clofibrate, for 8 days and then subjected to an acute
myocardial infarction by injecting them with two large doses of
isoproterenol spaced 24 hours apart. The animals were killed at sequential time intervals during the acute
necrosis and early repair phases of
myocardial infarction. Pre-treatment with
clofibrate caused a definite improvement in survival, less
shock and prostration, and ECG evidence of little or no
ischemia. Increased
SGOT levels, hepatic
lipid and
necrosis were indicative of advanced liver damage. Although
clofibrate-treated animals showed little change in serum
lipids during the acute cardiac
necrosis phase, they were hyperglycemic and showed the greatest increase in BUN levels.
Clofibrate-treated animals had higher serum
corticosterone levels than those given
isoproterenol alone. Despite superior survival rates, both the arteriosclerotic and non-arteriosclerotic,
clofibrate-treated animals exhibited equally severe histopathologic evidence of myocardial damage. It is suggested that the protective effect of prophylactic treatment with
clofibrate against
isoproterenol-induced
myocardial infarction in rats may be due to its ability to change
corticosterone levels in the circulation.