Some evidence for active constriction in the human pulmonary vascular bed.

T HE capacity of small pulmonary blood vessels for vasoconstriction remains a controversial subject.1 2 Evidence is accumulating which suggests that at least under abnormal circumstances vasoconstriction of the pulmonary vascular bed may occur.3 The following is a report on changes in pulmonary arteriolar resistance (PAR) during norepinephrine infusion based on simultaneous measurements of blood flow and pressures in the pulmonary vascular system. The pulmonary arteriolar resistance depends on the physical dimensions (geometry) of the vascular bed and on the viscosity of blood (Poiseuille-Hagen equation). If one assumes that the viscosity undergoes no measurable change during administration of norepinephrine, the decisive factor responsible for a change in resistance should be a change in radius of the small vessels. A rise in pulmonary artery pressure alone would tend to dilate vessels passively and to lower the pulmonary arteriolar resistance. An increase in this resistance in the presence of a rise in pulmonary artery pressure constitutes evidence for active vasoconstriction in the pulmonary vascular bed.