Effect of N-acetylcysteine on myocardial infarct size following ischemia and reperfusion in dogs.

The present study was designed to examine the role of N-acetylcysteine (NAC) on free radical mediated reperfusion injury in canine model. Fourteen dogs underwent 90 min of left anterior descending coronary artery (LAD) occlusion followed by 4 h of reperfusion. Treated animals received loading dose of NAC (250 mg/kg) at the time of reperfusion upto 1 h followed by maintenance dose (70 mg/kg) for remaining 3 h through left atrial line. Infarct size, myocardial tissue lipid peroxidation, superoxide dismutase (SOD) and glutathione (GSH) levels were measured at the end of reperfusion in treated (n = 7) and untreated animals (n = 7). Left ventricular end diastolic pressure was significantly lower in treated animals compared to untreated group. SOD and GSH levels in myocardial tissue at risk and in infarcted zone were similar in both groups. However, in NAC treated animals the lipid peroxidation was significantly lower in comparison to untreated control animals. Infarct size in the area at risk, percent left ventricular necrosis and myocardial tissue preservation were not significantly different in treated and untreated animals. These results suggests that N-acetylcysteine infusion at the time of reperfusion following 90 min of ischemia and 4 h of reperfusion fails to offer significant cardioprotection against free radical damage but it can improve ventricular performance by decreasing pre load.