Reappearance of myocytes in ovine infarcts produced by six hours of complete ischemia followed by reperfusion

Background. In this study we tested the hypothesis that delayed reperfusion of ischemic myocardium - too late to save myocytes - attenuates infarct ex pansion and improves collagen synthesis. Methods. The hypothesis was tested in a sheep model of anteroapical infarct ion that has no collateral blood now to the area at risk. After coronary li gation or arterial occlusion for 1 or 6 hours, sheep had serial hemodynamic and quantitative echocardiographic studies before and after infarction and 2, 5, 8, and 12 weeks later. Hearts were examined by light and electron mi croscopy at 2 and 12 weeks; hydroxyproline and ratios of type I/III collage n were measured at 12 weeks. Results. After coronary occlusion, left ventricular (LV) function progressi vely decreased and size increased to form an anteroapical aneurysm. After 1 hour of ischemia, neither resting LV size nor function changed; the infarc t contained a midmyocardial scar between epicardial and endocardial muscle. After 6 hours of ischemia, LV function was significantly better than that in nonperfused sheep. Two weeks after 6 hours of ischemia, no viable myocyt es were visible by light microscopy, but electron micrographs showed rare i ntact nucleated myocytes with scarce cytoplasmic myofibrils. At the 12th we ek epicardial and endocardial myocytes reappeared in the infarct. Infarct c ollagen type I/III ratios were 1.2 in reperfused groups and 0.7 in nonperfu sed sheep. Conclusions. Delayed reperfusion causes loss and subsequent reappearance of ovine epicardial myocytes, improves collagen type I/III ratios, and attenu ates LV dilatation and loss of function. One hypothesis to explain the reap pearance of myocytes is that reperfusion partially reverses an incomplete a poptotic process.