Myocardial changes were studied in dogs in an attempt to correlate the effects of anoxic cardiac arrest with subcellular changes, specifically those in mitochondria. Twenty dogs were studied to determine the effects of anoxia on mitochondria in hearts with chronic outflow obstruction produced by clamping the aorta. Two animals were used as normal and two as experimental controls. Except for normal controls, all dogs were placed under complete cardiopulmonary bypass, some under normothermic and some under hypothermic conditions. After 40 minutes of aortic occlusion at 37°C, animals showed depression of left-ventricular function as indicated by profound impairment of the oxidative phosphorylation process of the mitochondria. The difference between the respiratory control rates in experimental controls and the experimentals was significant at the p<0.001 level, demonstrating that cardioplegia of 40 minutes is detrimental to the canine heart through its effect on the mitochondrial activity. This deterioration was decreased by 33% if the temperature of the perfusion blood was kept at 30°C.