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.

Human pulmonary vascular response to 4 h of hypercapnia and hypocapnia measured using Doppler echocardiography

“…There is evidence from animal experiments that both alveolar PO 2 (PA O 2 ) and Pv O 2 affect pulmonary vascular tone (13,15). In the present experiment, Pv O 2 in the hypocapnia protocol was ϳ4 Torr lower than in the control and hypercapnia protocols (Fig.…”

Relation between Shunt, Aeration, and Perfusion in Experimental Acute Lung Injury

“…Although discrepancies in the literature could be partly related to differences in FI O 2 , inconsistencies regarding the effect of poorly aerated tissue, as defined by CT, on shunt or Pa O 2 persist among studies performed at similar FI O 2 , whether it is 1 (6,7,42,43) or less (5,9), indicating that differences in FI O 2 alone can not explain those discrepancies. It is possible that, had we used lower FI O 2 , shunt would have been less, because an FI O 2 of 1 is expected to promote resorption atelectasis (44) and blunt hypoxic pulmonary vasoconstriction in shunting regions through its effect on mixed venous PO 2 (45).…”

Ascites and venous carbon dioxide tensions in juvenile chickens of highly selected genotypes and native strains

“…Hypoxia, followed by hypoxemia (a reduced partial oxygen pressure in venous blood) exerts vasoconstriction in the lung of mammals and birds, which causes increased pulmonary arterial pressure and a higher workload of the right ventricle (Marshall and Marshall, 1983;Scheid and Holle, 1978). This response of vasoconstriction is accounted for by smooth muscle cells in the pulmonary arterial wall responding to the O 2 tension in its vicinity (Marshall and Marshall, 1983).…”

“…This response of vasoconstriction is accounted for by smooth muscle cells in the pulmonary arterial wall responding to the O 2 tension in its vicinity (Marshall and Marshall, 1983). Endothelin, which is produced by endothelial vascular cells during hypoxia is one of the most potent and long lasting vasoconstrictors known (Rakugi et al, 1990); a spectacular doseresponse relationship of the vasoconstriction effect of endothelin was found on human pulmonary artery branches (Yanagisawa et al, 1988).…”