Eplerenone is a competitive antagonist of the
aldosterone receptor with an additional PI3K-Akt activity. The existing cram has been intended to explore, whether
eplerenone treatment attenuates the expansion of
myocardial infarction in
isoproterenol treated rats by restoring hemodynamic, biochemical, and histopathological changes.
Isoproterenol induced
cardiotoxicity was evidenced by marked ST elevation, decrease in systolic, diastolic, mean arterial pressures. Maximal positive rate of developed left ventricular pressure (+LVdP/dt max, a
indicator of myocardial contraction), maximal negative rate of developed left ventricular pressure (-LVdP/dt max, a meter of myocardial relaxation) and an increase in left ventricular end-diastolic pressure (LVEDP, a marker of pre-load) were also shown. In addition, a significant reduction in activities of
myocardial creatine kinase-MB
isoenzyme,
lactate dehydrogenase,
superoxide dismutase,
catalase, and
reduced glutathione level along with increase in
malondialdehyde content were observed. Oral pre-treatment with
eplerenone (50, 100 and 150 mg/kg) daily for a period of 14 days, constructively modulated the studied parameters in
isoproterenol-induced myocardial injury. The protective role of
eplerenone on isoproterenolinduced myocardial damage was further confirmed by histopathological examinations.
Eplerenone at doses of 100 mg/kg and 150 mg/kg produced more pronounced protective effects than 50 mg/kg
body weight. Together, our study provides evidence for protective effects of
eplerenone on myocardium in experimentally induced
myocardial infarction.