Myocardial oxygen consumption and segmental shortening during selective coronary hemodilution in dogs.

Experiments were conducted in 33 open chest, anesthetized dogs to evaluate direct effects of hemodilution on myocardial oxygenation and contractile function. The left anterior descending coronary artery (LAD) was perfused selectively from a controlled pressure reservoir with either normal arterial blood or arterial blood diluted with lactated Ringer's solution. Systemic hemodynamic parameters were held stable. In the LAD bed, values were obtained for coronary blood flow (CBF) with an electromagnetic flowmeter, myocardial oxygen consumption (MVO2) using the Fick principle, and percentage segmental shortening (%SS), an index of local myocardial contractility, by sonomicrometry. Studies were conducted with LAD perfusion pressure (PP) set at control (100 mm Hg) and at 50% of that level to simulate coronary insufficiency (CI). CI abolished coronary reactive hyperemia after release of a 90-second occlusion, indicating exhausted vasodilator reserve capacity. With PP at control, reductions in LAD hematocrit to as low as 10% had no effect on MVO2 or %SS, because increases in blood flow were sufficient to offset induced falls in arteriovenous oxygen content difference. However, during CI, a more modest reduction in hematocrit to 17% caused reductions in both MVO2 and %SS, because of inadequate flow responses during hemodilution. The following conclusions can be made: 1) Extreme hemodilution is well tolerated by the normal heart with a stable work requirement and; 2) Relatively modest hemodilution may compromise myocardial oxygenation and contractile function when in the presence of exhausted or severely depleted vasodilator reserve capacity.