An Intrinsic Adrenergic Vasodilator Mechanism in the Coronary Vascular Bed of the Dog

The question of whether the coronary blood vessels contain an intrinsic adrenergic mechanism for vasodilatation has been examined by studying the response of the coronary vessels of the dog to isoproterenol. Initially, coronary blood flow, coronary sinus PO2, mean arterial pressure, and heart rate were measured continuously in anesthetized, open-chest animals. When isoproterenol, 0.1 to 0.3 μg/kg/min, was given intravenously, coronary flow and coronary sinus PO2 always increased in spite of tachycardia and a reduced or unchanged arterial pressure. Although this response suggested a primary vasodilating effect of isoproterenol, a vasodilatation consequent to increased myocardial activity or an extracardiac factor could not be eliminated. Accordingly, additional studies were performed in an isolated heart arrested with potassium and perfused with whole blood at constant rates of flow. Isoproterenol was given by single injections and constant infusions and always produced a decrease of perfusion pressure. These decreases could be blocked by nethalide and, as indicated by measurements of myocardial oxygen uptake and coronary venous PO2, did not depend upon increased myocardial metabolism or decreased myocardial oxygenation. With injections of 0.01, 0.1, 1.0, and 10.0 μg of isoproterenol, the decreases averaged respectively 3, 8, 14, and 26% of the control pressures. It is concluded that the coronary vessels of the dog do contain an intrinsic adrenergic mechanism for vasodilatation.