Transmural coronary venous O2 saturations in normal and isolated hearts.

Blood O2 saturations were measured by microscopic oximetry in the small coronary veins of wither open-chest or isolated and blood-perfused dog hearts. Subendocardial saturations (average 34%) were significantly lower than subepicardial (average 52%) in isolated hearts contracting isovolumically at systolic and coronary perfusion pressures of 100 mmHg. Saturations of botb regions fell and were not significantly different from each other (both averaged 16%) with partial coronary occlusion. When MVo2 was increased by calcium infusion, subendocardial saturations fell sharply to about 2% and were significantly, lower than subepicardial (average 10%). Conversely, when MVo2 was decreased by ventricular decompression, saturations rose equally in subendocardium (average 40%) and subepicardium (average 45%) (not significant). These data illustrate the efficacy of cascular autoregulation in isolated hearts. In open-chest dogs, as in isolated hearts with partial coronary occlusion, subendocardial (average 20%) saturations were not significantly diffenent from each other and ranged from 0 to 70%, suggesting the possibility of significant differences either in regional coronary flow or MVo2, or both, in closely adjacent areas throughout the myocardium.

The Anrep effect reconsidered.

Evidence is presented supporting the hypothesis that the positive inotropic effect after an abrupt increase in systolic pressure (Anrep effect) is the recovery from subendocardial ischemia induced by the increase and subsequently corrected by vascular autoregulation of the coronary bed. Major evidence consists of data obtained from an isolated heart preparation showing that the Anrep effect can be abolished with coronary vasodilation, and that with an abrupt increase in systolic pressure there is a significant reduction in the distribution of coronary flow to subendocardial layers of the ventricle. Furthermore, the intracardiac electrocardiogram shows S-T segment and T wave changes after an abrupt increase in ventricular pressure similar to that noted after coronary constriction. Major implications are that normally there may be ischemia of the subendocardial layers tending to reduce myocardial contractility which may account, in part, for the positive inotropic effect of various coronary vasodilators; that with an abrupt increase in ventricular pressure the subendocardium is rendered temporarily ischemic, placing the heart in jeopardy from arrhythmias until this is corrected; and that end-diastolic pressure and the intracardiac electrocardiogram may provide a means of evaluating the adequacy of circulation to subendocardial layers in diseased ventricles when systolic pressure is abruptly increased.

Left ventricular performance and coronary flow after coronary embolization with plastic microspheres.

Coronary flow, left ventricular circumference, and left ventricular pressure were observed in the isovolumically contracting, isolated canine heart supported with arterial blood from a donor. Systolic pressure, heart rate, and coronary perfusion pressure were held constant while the coronary bed was progressively embolized with either large (average 865 mu) or small (average 10 mu) polystyrene microspheres. During embolization with large microspheres, coronary flow diminished progressively. After sufficient embolization, decreased ventricular performance was indicated by a rise in end-diastolic pressure. During embolization with small microspheres, coronary flow initially increased, which suggests the effective release of a vasodilator substance. Return of coronary flow to control levels occurred only after the end-diastolic pressure rose, on the average, to above 30 mm Hg. After embolization with both sizes of microspheres, ventricular diastolic pressure-volume relationships showed decreased ventricular compliance. This was attributed, in part, to edema of the ventricular wall and, in part, to focal shortening of the sarcomeres where the circulation was compromised. Embolization with both sizes of microspheres ultimately caused a decrease in ventricular performance, although when the systolic pressure was increased the usual relationship between peak developed wall stress, and end-diastolic pressure showed less of a descending limb than that found in the nonembolized, isolated heart. It is felt that the data summarized above have bearing on ventricular performance and coronary flow in clinical situations where hearts are perfused through pump oxygenator systems and are thereby subject to embolization from aggregated clumps of platelets and fibrin.