Influence of repetitive coronary occlusions on myocardial adenine nucleosides, high energy phosphates and ultrastructure

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Abstract
We compared the effects of repeated short periods of myocardial ischemia with those of permanent occlusion (canine open-chest) with regard to tissue content of adenine nucleotides, nucleosides, creatine phosphate, and ultrastructure. Coronary occlusion for 3 min followed by a reperfusion period of 7 min was repeated up to a cumulative occlusion time of either 45 or 90 min. After cumulative occlusions of 15, 30, 45, and 90 min, transmural needle biopsies were taken from the ischemic area to be analyzed for adenine nucleotides, nucleosides, creatine phosphate, and ultrastructural changes. At the end of each experiment, tetrazolium salt staining was used for macroscopic detection of myocardial necrosis. These data were obtained with those obtained from dogs with a permanent coronary occlusion of 45 and 90 min, respectively. After repeated coronary occlusions at a cumulative occlusion time of 45 min, macroscopic detection of necrosis was negative, and after 90 min of cumulative coronary occlusion, patchy subendocardial tissue necrosis was found in only one out of 13 dogs, whereas in the group with permanent coronary occlusion, small patchy subendocardial necrosis was found in 95% after 45 min, and after 90 min permanent coronary occlusion, large subendocardial necrotic areas spreading towards the epicardial layers were found in 90% of the hearts. Ultrastructural investigations showed only slight to moderate ischemic injury after 45 and 90 min intermittent coronary occlusion, whereas permanent coronary occlusion produced moderate to severe ischemic injury after 45 min; and 90 min permanent coronary occlusion produced irreversible ischemic injury in all subendocardial tissue samples and in 80% of the subepicardial tissue samples. ATP content was decreased significantly less during intermittent coronary occlusion compared with that during permanent coronary occlusion. AMP and nucleosides did accumulate during permanent occlusion but not with repetitive brief coronary occlusions. Our results show that intermittent reperfusion significantly delays ischemic injury in comparison with permanent coronary occlusion.

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