Determinants of regional myocardial oxygen supply in the left ventricle. An experimental study in the in situ working canine heart.

The main factors that regulate myocardial oxygen supply include the 1. coronary blood flow controlling the volume flow fraction of red cells, 2. the oxygen carrying capacity of capillary blood dependent on the red cell volume fraction occupying the capillaries, and 3. the density of perfused capillaries affecting the capillary diffusion capacity and the diffusion distance in the tissue. Differences exist between the inner and outer layers of the left ventricle that include differences of systolic and possibly diastolic tissue stresses and oxygen consumption. The highest values were observed in the vicinity of the left ventricular cavity. The regional differences of myocardial oxygenation were studied in anaesthetized open-chest dogs by measuring the myocardial perfusion rate, the microvascular hematocrit, the PS-product of 51Cr-EDTA, and the microvascular blood volume across the left ventricular wall in the heart working in situ. Gradients of blood flow rates were present with the highest flow in deep myocardial layers. Maximally increasing the coronary blood flow at normal perfusion pressure and metabolic load did not change the distribution of blood flow between subendocardial and subepicardial layers. Distal to a coronary stenosis, blood flow was markedly reduced and redistributed away from the subendocardial layers, indicating a relatively severe decrease of fractional red cell flow to the left ventricular myocardium. The microvascular dynamic hematocrit, i.e. the volume fraction of red cells, was evenly distributed across the left ventricular wall, but consistently reduced to 75 per cent of great vessel hematocrit. The maximal increase of coronary blood flow provoked a further reduction of microvascular hematocrit due to a decrease of the red cell volume, possibly by shunt flow of red cells through low resistance vessels of capillary size. At restricted coronary inflow, the microvascular hematocrit was decreased with a redistribution of red cells away from deep myocardial layers. Extern compression of microvessels by the tissue pressure, phase-separation between red cells and plasma at microvascular bifurcations, or decrease of the red cell fluidity may all contribute to this change. Reduction both of microvascular red cell flow fraction and the hematocrit diminishes the red cell flux within capillaries and decreases the ability of blood to deliver oxygen to the tissue, and more so in the subendocardial layers.(ABSTRACT TRUNCATED AT 400 WORDS)