Some Regulatory Mechanisms of the Human Pulmonary Vascular Bed

Abstract

Pulmonary blood volume was estimated by means of rapidly successive injections of an indicator into the pulmonary artery and left atrium with sampling of blood from a systemic artery. In 40 patients with mitral valve disease and in 4 patients with mild aortic valve disease, this volume was found to range from 122 to 455 ml/M2, with a mean of 233 ml/M2. Changes induced in pulmonary blood volume by physiologic maneuvers and pharma-cologic agents were correlated with changes in intravascular distending pressure to deduce active or passive vasomotion in the pulmonary circuit. Exercise, rapid intravenous infusion or methoxamine were found to cause passive pulmonary vasodilation manifested by a concordant rise in both pulmonary blood volume and intravascular distending pressure. Hexamethonium or vasovagal reactions induced passive narrowing, reflected by simultaneous reduction in both pulmonary blood volume and distending pressure. During acute hypoxia or angiotensin infusion, active constriction of the pulmonary vascular bed was evidenced by an increase in distending pressure but a decrease or no change in the pulmonary blood volume. During acetylcholine infusion, active dilation of the pulmonary vascular bed was reflected by a decrease in distending pressure but an increase in the pulmonary blood volume. However, with a given intervention, the change in the calculated pulmonary vascular resistance was variable. This study has demonstrated that the pulmonary blood vessels in unanesthetized man can be affected by both active and passive mechanisms and that changes in pulmonary vascular resistance cannot necessarily be equated with change in pulmonary vascular caliber.