Reduced Availability of Energy Initiates Pulmonary Vasoconstriction

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Abstract
The mechanism responsible for initiating hypoxic pulmonary vasoconstriction (HPV) remains controversial. In this study, reversible constriction of the pulmonary artery was produced when the ratio of carbon monoxide to oxygen was increased, demonstrating that HPV would be imitated even in the presence of a constant oxygen tension. Isolated rat lungs from 14 adult rats were perfused with a 5% albumin-physiological salt solution and ventilated with 21% O2, 5% CO2, balance N2. At the end of a 30-min stabilization period, the lungs were injected with a bolus of angiotensin II (0.2 .mu.g). They were then challenged three times for 5 min with an hypoxic gas mixture alternating with 5 min of normoxia. The ventilatory circuit was then changed to one in which 10% O2, 5% CO2 and varying concentrations of CO (balance N2) could be administered. The concentration ratios of CO:O2 were 0.5:1, 1:1, 2:1, 4:1, and 8:1. These were randomly administered for 6 min interspersed with 6 min of normoxia; a final angiotensin II challenge was given. The results show a slight but significant vasodilation with CO:O2 of 0.5:1, 1:1 with mean depressor responses of -0.7 .+-. 0.1, -0.7 .+-. 0.1 cm H2O and progressive vasoconstriction with CO:O2 of 2:1, 4:1, 8.5:1 with mean pressor responses of 0.11 .+-. 0.3, 4.0 .+-. 0.4 and 6.2 .+-. 0.5 cm H2O. The pressor response to angiotensin II remained unchanged from beginning to end (9.5 .+-. 0.5, 8.1 .+-. 0.7 cm H2O). The pressor responses, therefore, are consistent with reduced function of the cytochromes of the electron transport chain. These results suggest that HPV may be initiated by a reduction of energy state of the vascular smooth muscle and that postulation of a specific oxygen receptor is not necessary.

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