Nonsustained pulmonary vasoconstriction during acute hypoxia in anesthetized dogs.

Abstract

The objectives of this study were to describe in greater detail the initial rise and spontaneous decline in acute hypoxic pulmonary vasoconstriction and to investigate a number of mechanisms that could have caused this secondary vasodilation. With the onset of isocapnic hypoxia (Pao2 of 28, 44, or 56 mmHg), pulmonary vascular resistances increased to maximum values at 3 min and then spontaneously declined toward control values. Pulmonary perfusion pressures rose to maxima at approximately 4 min and then also declined. During severe hypoxic exposures (Pao2 of 30-37 mmHg) this secondary vasodilation was found not to be due to beta-adrenergic-induced vasodilation, withdrawal of alpha-adrenergic-induced vasoconstriction, vasodilation caused by a sustained increase in pulmonary blood flow, fatigue of the vascular smooth muscle contractile mechanism, or release of vasodilatory prostaglandins. It is suggested that the decline in hypoxic pulmonary vasoconstriction may be due to an exhaustion of a chemical mediator, release of a pulmonary vasodilator agent, or myogenic stress relaxation.