During operations employing cardiopulmonary bypass the coronary collateral circulation protects regions of myocardium distal to obstructed coronary vessels. The physiology of the coronary collateral bed during cardiopulmonary bypass has not been elucidated. These studies investigate the physiology of the coronary collateral bed. By understanding responses of these collaterals during cardiopulmonary bypass, it will be possible to afford better protection to ischemic regions of myocardium during cardiac procedures designed specifically to relieve ischemic heart disease. Application of such information may reduce the perioperative infarction rate and mortality associated with those procedures and contribute to prolonging survival in patients undergoing these operations. The studies employ a canine model in which a collateral vascular bed is created by gradual occlusion of an ameroid constrictor on the circumflex coronary artery. During total cardiopulmonary bypass changes in blood supply and function of the collateral bed are compared with the normal region of myocardium supplied by the unobstructed left anterior descending coronary artery. The basic physiology of the collateral bed under conditions of extracorporeal circulation are defined by examining properties of autoregulation, critical closing pressure, post-ischemic hyperemia, and pharmacologic vasoconstriction and vasodilatation. These studies will then be extended to examine how alterations in the contractile state of the myocardium, commonly produced during cardiac bypass procedures, affect the physiology of the coronary collateral circulation. Such changes will include ventricular fibrillation, pharmacologic cardioplegia, and hypothermia. The effects of hemodilution will also be assessed. The final aspect of the study is the correlation between changes in regional flow and function with histologic evidence of myocardial injury. The primary methods to be used are tracer microspheres for determining coronary collateral blood flow and sonar micrometry for determining regional functional changes. Myocardial injury will be assessed by standard histologic techniques and by uptake of labelled pyrophosphate.