Possible Role Of Nitric Oxide In The Cardioprotective Actions Of Enalapril And Lisinopril In Rats
ACE inhibitors are effective in the treatment of ischemia and reperfusion-induced myocardial infarction. It was reported that in hypercholesterolemic state, myocardial infarction was more. This may be due to decreased synthesis or release of nitric oxide (NO) or enhanced degradation of NO in the coronary bed in hypercholesterolemic state. Hence the cardioprotective effects of enalapril and lisinopril were studied along with L-arginine (NO donor) in hyperchloesterolemic rats. Myocardial infarction was produced by occlusion of left coronary artery for 30 min followed by 4 h of reperfusion. Infarct size was measured by using triphenyl tetrazolium chloride (CTTC) stain method. Infarct size, expressed as percent left ventricle necrosis (PLVN) was found to be significantly reduced with lisinopril and enalapril in normal rats as compared to control untreated animals, the degree of cardioprotection offered by enalapril and lisinopril was reduced in hyperchloesterolemic rats. When ACE inhibitors are combined with NO donor L-arginine, the degree of cardioprotection was improved in hyperchloesterolemic rats. These results suggest a possible role of NO in cardioprotection mediated by ACE inhibitors.