Site and sensitivity for stimulation of hypoxic pulmonary vasoconstriction.

Abstract

Rat lungs were perfused in an in vitro circuit with separate control of alveolar and pulmonary arterial O2 tension. With perfusion flow constant, the hypoxic pulmonary vasoconstrictor (HPV) response was measured as changes of perfusion pressure. HPV was a function of both alveolar O2 tension (PvO2) and was described by a double sigmoid response surface. Where RA-v is this pressure response expressed as a percent of the maximum, the linearized form of the response surface is given by log [RA-v/(100-RA-v)] = 3.93 - 1.029 (log PvO2) - 1.623 (log PAO2). From this relationship it was concluded that 1) HPV is determined by PAO2 and PvO2; 2) the fundamental stimulus-response relationship is a sigmoid with a 50% response when both PAO2 and PvO2 are 30.3 Torr; 3) PAO2 has a greater effect than PvO2 due in part to the geometry of the vascular wall but principally due to O2 exchange between alveolar gas and blood in small pulmonary arteries; 4) there is not a localized sensor for HPV (the response is accounted for by each smooth muscle cell in the pulmonary arterial wall responding to the O2 tension in its vicinity); and 5) the characteristics of the response suggest that the cell sensor resembles a cytochrome.