Progression of myocardial necrosis during reperfusion of ischemic myocardium

Background-The occurrence of myocyte necrosis during reperfusion of ischemic myocardium is controversial. This study measured myocardial 2-deoxyglucose uptake, correlated with histology, to determine whether loss of viability occurred during reperfusion of ischemic myocardium. Methods and Results-In 12 anesthetized dogs, the left anterior descending coronary artery was occluded for 90 minutes before 4 hours reperfusion. Myocardial blood now was measured by microspheres and the tracers C-14-2-deoxyglucose and F-18-2-deoxyglucose were injected intravenously after 5 and 180 minutes of reperfusion, respectively, After 240 minutes, the heart was stained with thioflavin-S (size of no-renew zone) and triphenyl-tetrazolium chloride (TTC, extent of necrosis), Samples from normal, salvaged, and necrotic myocardium were counted for C-14- and F-18-deoxyglucose and microspheres, With the use of a three-compartment model of 2-deoxyglucose uptake, the rate constant k(3) for phosphorylation of C-14- and F-18-2-deoxyglucose was calculated for each sample, Viability was defined as k(3) greater than or equal to 0.125 min(-1) (predictive accuracy 88% versus electron microscopy and 97% versus TTC), Among 58 samples from no-renew regions, 97% were nonviable after 5 minutes of reperfusion (k(3)=0.096+/-0.027 min(-1)). Among 164 samples from salvaged myocardium, 95% were viable after both 5 and 180 minutes of reperfusion (k(3)=0.170+/-0.056 min(-1) P<.01 versus no-reflow), Among 179 samples from infarcted myocardium, mean k(3) after 5 minutes of reperfusion was 0.184+/-0.070 min(-1) and 65% of samples were viable, but after 180 minutes of reperfusion mean k(3) had decreased to 0.077+/-0.032 min (P<.0001) and 98% of samples were nonviable, Conclusions-A large proportion of samples from infarcted myocardium are viable at the end of the ischemic period but lose viability during the first hours of reperfusion.