Oxygen transport to the canine left ventricle distal to a flow-limiting coronary artery stenosis.

Myocardial blood flow, microvascular blood volume and red cell volume fraction (hematocrit) were investigated on a regional basis distal to the site of a coronary artery constriction in the left ventricular myocardium of anaesthetized open-chest dogs. Myocardial oxygen consumption was computed with the Fick equation. After application of the coronary artery stenosis myocardial blood flow decreased from 76.6 +/- 8.4 to 36.6 +/- 6.6 ml X min-1 X 100 g-1 in subepicardial layers and from 90 +/- 6.9 to 24.1 +/- 6.5 ml X min-1 X 100 g-1 in subendocardial layers of the left ventricular wall with a significant redistribution of blood flow away from the subendocardium. The red cell volume decreased significantly from 1.27 +/- 0.07 to 0.95 +/- 0.07 ml X 100 g-1 in subepicardial layers and from 1.52 +/- 0.09 to 1.01 +/- 0.11 ml X 100 g-1 in subendocardial layers of the left ventricle, whereas the plasma volume increased slightly but not significantly. In the subepicardial layers the plasma volume increased from 2.84 +/- 0.11 to 3.40 +/- 0.21 ml X 100 g-1 and in the subendocardial layers from 3.24 +/- 0.09 to 3.76 +/- 0.22 ml X 100 g-1. Coronary capillary density as reflected in measurements of microvascular blood volume (red cell volume + plasma volume) did not change significantly. The microvascular hematocrit (red cell volume/red cell volume + plasma volume) was uniformly distributed in both myocardial layers. The average hematocrit of the microcirculation during control flow rate (31 +/- 1%) was consistently lower than hematocrit drawn from large arteries. Expressed relatively to the hematocrit in arterial blood, the microvascular hematocrit was found to be in the order of 0.75. Distal to the flow-limiting coronary artery constriction, mean microvascular hematocrit fell significantly to 23 +/- 1%. During impeded coronary inflow, the myocardial oxygen consumption fell significantly from 3.3 +/- 0.6 to 2.0 +/- 0.4 ml X min-1. These results indicate that during ischemia, the myocardium is not only suffering from a diminished blood supply, but also is perfused by blood with a diminished oxygen delivery capacity.