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 flow was measured by microspheres and the tracers 14C-2-deoxyglucose and 18F-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-reflow zone) and triphenyl-tetrazolium chloride (TTC, extent of necrosis). Samples from normal, salvaged, and necrotic myocardium were counted for 14C- and 18F-deoxyglucose and microspheres. With the use of a three-compartment model of 2-deoxyglucose uptake, the rate constant k3 for phosphorylation of 14C- and 18F-2-deoxyglucose was calculated for each sample. Viability was defined as k3> or = 0.125 min(-1) (predictive accuracy 88% versus electron microscopy and 97% versus TTC). Among 58 samples from no-reflow regions, 97% were nonviable after 5 minutes of reperfusion (k3=0.096 +/- 0.027 min[-1]). Among 164 samples from salvaged myocardium, 95% were viable after both 5 and 180 minutes of reperfusion (k3=0.170 +/- 0.056 min[-1] P<.01 versus no-reflow). Among 179 samples from infarcted myocardium, mean k3 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 k3 had decreased to 0.077 +/- 0.032 min(-1) (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.
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 flow was measured by microspheres and the tracers 14C-2-deoxyglucose and 18F-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-reflow zone) and triphenyl-tetrazolium chloride (TTC, extent of necrosis). Samples from normal, salvaged, and necrotic myocardium were counted for 14C- and 18F-deoxyglucose and microspheres. With the use of a three-compartment model of 2-deoxyglucose uptake, the rate constant k3 for phosphorylation of 14C- and 18F-2-deoxyglucose was calculated for each sample. Viability was defined as k3> or = 0.125 min(-1) (predictive accuracy 88% versus electron microscopy and 97% versus TTC). Among 58 samples from no-reflow regions, 97% were nonviable after 5 minutes of reperfusion (k3=0.096 +/- 0.027 min[-1]). Among 164 samples from salvaged myocardium, 95% were viable after both 5 and 180 minutes of reperfusion (k3=0.170 +/- 0.056 min[-1] P<.01 versus no-reflow). Among 179 samples from infarcted myocardium, mean k3 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 k3 had decreased to 0.077 +/- 0.032 min(-1) (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.