Anatomical and Chemical Changes in the Myocardium Following Short-Term Coronary Artery Occlusion in Dogs *

Following permanent ligation of the anterior descending ramus of the left coronary artery in dogs, from 7 to 9 hours must elapse before anatomical injury can be demonstrated histologically.5' 6, 7 When occlusion of the coronary artery was maintained for from 30 minutes to 8 hours and the dog was sacrificed 2 hours after the restoration of circulation, edema of the interstitial tissue was present after >2 hour of ischemia, and by the end of 2 hours, exudate, necrosis of the myocardial fibers, and extensive hemorrhage had developed.7 Functional studies of regions of ischemic myocardium by optical myographic methods', 8 indicated an immediate impairment of muscular activity following ligation of the coronary artery with complete abolition of contractions in the affected muscle in 1 to 1 2 minutes. The prompt asphyxial arrest of myocardial contraction leads to the consideration of the role of glycogen and its breakdown-product lactic acid in the anaerobic activity of the myocardium. Lactic acid in the anoxemic muscle after coronary occlusion of from 30 minutes to 24 hours is increased by 100 to 200 per cent, while the glycogen concentration is markedly decreased.' Occlusion of the coronary artery for from 2 to 8 hours, with subsequent restoration of circulation for 2 hours, showed no significant difference in the lactic acid content of the ischemic and control zones, while the glycogen content of the ischemic zone continued low, as in the simple ligation experiment.7 The accumulated lactic acid was washed out apparently by the reestablished blood flow. The failure of glycogen resynthesis in these experiments is further evidence of severe myocardial injury. Asphyxial arrest of the contraction of the frog heart has been studied by Clark, Gaddie, and Stewart.1 They concluded that contraction continues as long as formation of lactic acid continues, and