Myocardial blood flow and its distribution in anesthetized polycythemic dogs.

Abstract

Decreased cardiac output, coronary blood flow and systemic O2 transport in polycythemia are attributed to increased blood viscosity and regarded as potentially harmful. The effects of isovolemic polycythemia on these variables and on myocardial O2 consumption and regional myocardial blood flow were studied in 31 anesthetized dogs, 7 with cannulated left main coronary arteries. Measurements were made at rest, during hypoxemia or adenosine infusions, and with aortic stenosis, pacing or an aorto-atrial fistula. When hematocrit increased from 42%-66%, it reduced cardiac output by 36% and systemic O2 transport by 8%. With hypoxemia, cardiac output rose in polycythemic dogs. Normoxemic polycythemia decreased myocardial blood flow by 46% and increased mean coronary resistance by 54%, slightly decreased myocardial O2 transport and consumption, and did not alter coronary sinus O2 tension or myocardial O2 extraction. Cardiac stress, hypoxemia and adenosine infusion lowered coronary resistance in polycythemic dogs. Left ventricular myocardial O2 transport was dependent on pressure work and not on arterial O2 content or hematocrit. With maximal coronary vasodilation, coronary vascular resistance at hematocrits of 66% was 1.5 times that at 42%. Polycythemia per se did not alter the even distribution of flows across the left ventricular wall, but subendocardial underperfusion began at higher perfusion pressures in polycythemic than in normocythemic dogs. Autoregulation apparently plays a role in regulating flows and O2 transport in polycythemia. With maximal coronary vasodilation, however, the increased viscosity of polycythemic blood could be an important factor reducing the amount of myocardial blood flow and O2 transport.