Pulmonary vasomotor responses in the cat; the effects and interrelationships of drugs, hypoxia and hypercapnia.

Abstract

In anæsthetized artificially‐ventilated cats, one lobe of a lung was perfused at a constant rate of flow with arterial blood. Under these conditions changes in pulmonary arterial pressure at end‐expiration, in the absence of significant changes in left atrial pressure, were assumed to indicate changes in pulmonary vascular resistance. Hypoxia and hypercapnia, produced by changing the ventilating gas mixture, caused increases in pulmonary vascular resistance. Infusion into the pulmonary artery of noradrenaline, dopamine, histamine and 5‐hydroxytryptamine caused increases in pulmonary vascular resistance, and infusions of isopropylnoradrenaline caused decreases. The β blocking agent propranolol caused increases in pulmonary vascular resistance, and the α blocking agent phentolamine caused decreases. Propranolol reduced the pulmonary vasodilator action of isopropylnoradrenaline. Phentolamine temporarily reduced or abolished the actions of noradrenaline, dopamine and histamine on the pulmonary circulation; the action of 5‐hydroxytryptamine was less affected. Phentolamine reduced or abolished the action of hypoxia for a period corresponding to that in which the actions of catecholamines and histamine were reduced. The histamine‐liberating substance BW 48/80, in addition to causing effects attributable to histamine‐release, had effects similar to phentolamine; it temporarily reduced the actions of hypoxia, noradrenaline, dopamine and histamine on the pulmonary circulation; the action of 5‐hydroxytryptamine was less affected. The action of hypoxia was not reduced by bretylium; after mepyramine it was not abolished but was sometimes slightly reduced.