The “no-reflow” phenomenon after temporary coronary occlusion in the dog

the genesis of the "no-reflow " phenomenon was investi-gated in the left ventricular myocardium of dogs sub-jected to temporary occlusions of a major coronary ar-tery for 40 and 90 min. Intravenous carbon black or thioflavin S (a fluorescent vital stain for endothelium) were used to demonstrate the distribution of coronary arterial flow in control and damaged myocardium. These tracers were injected simultaneously with re-lease of the coronary occlusion or after 5 or 20 min of reflow of coronary arterial blood. After 40 min of ischemia plus arterial reperfusion, usually the tracers were evenly distributed throughout the damaged tissue at each time of reperfusion. On the other hand, when reflow was allowed after 90 min of ischemia, portions of the inner half of damaged myocardium were not pene-trated by the tracers. Electron microscopic study of this poorly perfused tissue revealed severe capillary damage; endothelial cells with large intraluminal protrusions and decreased pinocytic vesicles were common. Also, oc-casional intraluminal fibrin thrombi were noted, as well as extravascular fibrin deposits and erythrocytes. Myo-cardial cells were swollen in both poorly perfused and well-perfused irreversibly injured tissue. Contraction bands and mitochondrial Ca"+ accumulation were promi-nent features of irreversible injury with reflow at 40 min but were not noted after 90 min of ischemia in areas with poor perfusion. These results suggest that 40 min of ischemia were tolerated by the capillary bed of the dog heart without serious capillary damage or per-fusion defects, but that 90 min of ischemic injury was associated with the "no-reflow " phenomenon, i.e., fail-ure to achieve uniform reperfusion. This failure of re-flow was associated with extensive capillary damage and myocardial cell swelling. Death of severely ischemic myo-Mr. Kloner was a predoctoral fellow during the time o