Myocardial salvaging effect of telmisartan in experimental model of myocardial infarction.

Telmisartan is a unique angiotensin II receptor blocker with an additional peroxisome proliferator-activated receptor-gamma (PPAR-gamma) activity. The present study has been designed to investigate whether telmisartan treatment attenuates the development of acute myocardial infarction in isoproterenol-treated rats by restoring hemodynamic, biochemical, histopathological and ultrastructural changes. Isoproterenol-induced cardiotoxicity was evidenced by marked decrease in systolic, diastolic, mean arterial pressures, maximal positive rate of developed left ventricular pressure (+LVdP/dt(max), a marker of myocardial contraction), maximal negative rate of developed left ventricular pressure (-LVdP/dt(max), a marker of myocardial relaxation) and an increase in left ventricular end-diastolic pressure (LVEDP, a marker of pre-load). In addition, a significant reduction in activities of myocardial creatine kinase-MB (CK-MB) isoenzyme, lactate dehydrogenase (LDH), superoxide dismutase (SOD), catalase, and reduced glutathione (GSH) level along with increase in malondialdehyde (MDA) content were observed. Oral pretreatment with telmisartan (1, 5 and 10mg/kg body weight) daily for a period of 14 days, favourably modulated the studied parameters in isoproterenol-induced myocardial injury. In addition, the protective role of telmisartan on isoproterenol-induced myocardial damage was further confirmed by histopathological and ultrastructural examinations. Telmisartan at a dose of 10mg/kg produced more pronounced protective effects than the other two doses (1 and 5mg/kg body weight). Present study thus provides evidence for protective effects of telmisartan on myocardium in experimentally induced myocardial infarction.