The Effects of Blood Pressure and Arterial Oxygen Saturation on the Myocardial Reactive Hyperemia

The effects of blood pressure and arterial oxygen saturation on the characteristics of the myocardial reactive hyperemia were studied in anesthetized open-chest dogs. Lowering blood pressure by means of graded hemorrhage, the reactive hyperemic flow decreased in proportion to the level of blood pressure. At a blood pressure level of 70 to 80mm Hg, the flow repayment decreased under 100%. Further lowering blood pressure to 60mm Hg, the reactive hyperemia almost disappeared. This decreased flow repayment did not recover in spite of the increase in blood pressure produced by blood transfusion, when blood pressure was once lowered to 60mm Hg or less. When arterial oxygen saturation was lowered by the decrease in the ventilatory volume, the decrease in the flow repayment paralleled to the fall in arterial oxygen saturation. The flow repayment did not reach 100% at the arterial oxygen saturation level of 60%. These results revealed that the myocardial reactive hyperemia was regulated by both metabolic and hemodynamic factors. When metabolic and hemodynamic conditions changed over the limiting level, the flow repayment did not attain 100% and the flow debt was not repaid completely. Further on the condition of the shock level, these changes in the repayment became irreversible and the metabolic regulation in the reactive hyperemia was lost.