CORONARY CIRCULATION RESPONSE TO HYPEROXIA AFTER VAGOTOMY AND COMBINED ALPHA AND BETA ADRENERGIC RECEPTORS BLOCKADE IN ANESTHETIZED INTACT DOG

In closed-chest vagotomized dogs with alpha and beta adrenergic receptors blockade, ventilation with 100 per cent oxygen at atmospheric pressure did not modify the tension-time index nor the myocardial oxygen consumption. However, coronary blood flow decreased and coronary resistance increased significantly. A rise of the myocardial pO2 was not likely to be primarily responsible for the elevation of the coronary resistance. Since in the presence of a fixed oxygen consumption the myocardial pO2-elevation would occur following the rise of the arterial pO2 whose direct effect on the vascular smooth muscle tone has been demonstrated in vitro by other workers, it may be concluded that elevation of arterial pO2 exerted a direct constrictive action on the coronary vessels. However, oxygen transport to the left ventricle remained commensurate to the myocardial oxygen consumption. It is suggested that an additional mechanism adjusted the elevated coronary resistance. Shifts of the myocardial pO2, resulting from transient imbalances between oxygen supply and demand, may be the stimulus initiating the adjustment through changing release of vasodilator or vasoconstrictor substances. Results of this paper and those previously published indicated that autonomic influences normally play a dominant role in the hyperoxia-induced reduction in cardiac work and metabolism. © 1969 Springer-Verlag.