Acute and Chronic Effects of Normothermic Anoxia on Canine Hearts

In order to evaluate the acute and chronic effects of normothermic cardiac anoxia, structural and functional observations were made on the hearts of 29 dogs subjected to total cardiopulmonary bypass. Elective, normothermic cardiac arrest was induced by aortic cross-clamping for 30 minutes in 7 dogs and for 45 minutes in 16 dogs. The remaining six dogs, which served as controls, were placed on bypass without aortic cross-clamping. The six control dogs and six of seven dogs subjected to 30 minutes of cardiac anoxia showed excellent cardiac function and minimal myocardial damage; one dog in the latter group that died 6 to 12 hours after bypass showed no myocardial damage. All 16 dogs subjected to 45 minutes of cardiac anoxia showed extensive myocardial damage. Depressed cardiac function was demonstrated in three of five dogs that survived for eight days or longer after bypass. The acute cardiac damage was of the myofibrillar degeneration type and progressed to replacement fibrosis; this damage was selectively localized in the left ventricular papillary muscles and subendocardium.