Some regulatory mechanisms of the human pulmonary vascular bed.

THERE IS still a question regarding the presence of active mechanisms of control for the pulmonary vessels in man. The controversy continues, since evidence for active vasomotion has usually been indirect. Because, in the past, it has been assumed that changes in pulmonary vascular resistance necessarily reflect changes in pulmonary vascular caliber, workers have drawn conflicting conclusions from similar experimental results. Recent excellent reviews summarize the present concepts.1-5 The caliber and, therefore, the volume of a vessel depend on (a) the transmural pressure and on (b) the distensibility of its wall. As defined by Burton,5 transmural pressure is the difference between the distending pressure inside and the tissue pressure outside the vessel. Vascular distensibility depends on mural elasticity as well as on active tension or muscular tone. Theoretically, passive changes in vascular caliber would be associated with concordant changes in pulmonary blood volume and transmural distending pressure, i.e., they would rise together or fall together. Thus, passive narrowing would be associated with a fall both in distending pressure and pulmonary blood volume, whereas passive dilation would be associated with a rise in both these parameters. These changes could occur with-