Coronary circulation response to hyperoxia after vagotomy and combined alpha and beta adrenergic receptors blockade in the anesthetized intact dog
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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 myocardialpO2 was not likely to be primarily responsible for the elevation of the coronary resistance. Since in the presence of a fixed oxygen consumption the myocardialpO2-elevation would occur following the rise of the arterialpO2 whose direct effect on the vascular smooth muscle tone has been demonstratedin vitro by other workers, it may be concluded that elevation of arterialpO2 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 myocardialpO2, 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.
Key-WordsBlood Oxygen Tension Coronary Blood Flow Coronary Resistance Myocardial Oxygen Consumption Adrenergic Receptors Blockade
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