Demonstration of the "no-reflow" phenomenon in the dog heart after temporary ischemia.

The effect of 40- or 90-min periods of temporary myocarardial ischemia on the distribution of coronary flow and capillary structure were assessed in groups of mongrel dogs. Thioflavin S. a fluorescent dye which stains vascular endothelium when injected intravenously, was used to demonstrate the distribution of microvascular perfusion at 10 sec, 5 min, or 20 min following release of a 40-or 90min circumflex coronary artery occlusion. Hearts which demonstrated perfusion defects were sampled for electron microscopy. Following 40 min of occlusion, thioflavin S was distributed uniformly throughout the myocardium. In contrast, following 90-min periods of coronary occlusion, perfusion defects always were present in the subendocardial half of the posterolateral left ventricular wall. Several morphological features in these areas of no reflow were observed by electron microscopy, including decreased endothelial pinocytotic vesicles, endothelial gaps and bleb formation, capillaries packed with erythrocytes, occasional intraluminal thrombi, and extravascular erythrocytes and fibrin. Myocardial cells showing severe injury always were seen within but also extended beyond the areas of poor perfusion. These results demonstrate that areas of no reflow occur following 90-min periods of ischemic injury in the dog, but that primary myocardial cell injury occurs during the ischemic period and not as a function of the "no-reflow" phenomenon.