Hypoxic pulmonary vasoconstriction and endogenous prostaglandin (PG) and thromboxane (TX) release in anesthetized pigs.

Products of the arachidonate cascade are known to be released from pulmonary tissue in normal and abnormal states, contributing to the regulation of pulmonary vascular resistance. To what extent hypoxic pulmonary vasoconstriction is affected by prostaglandin imbalances is still controversial. To evaluate PG and TX release, we measured plasma levels of TXA2, PGI2, PGF2a, and 13,14-dihydro-15-keto-PGF2a in healthy pigs undergoing normobaric hypoxic ventilation. Plasma levels of TXA2, PGI2, and PGF2a did not change during 10 minutes of hypoxia, whereas 13,14-dihydro-15-keto-PGF2a, the stable metabolite of PGF2a, was significantly elevated after 2, 5 and 10 minutes. Hemodynamic parameters showed an increase in heart rate and pulmonary vascular resistance. Our results suggest that alveolar hypoxia releases PGF2a from lung tissue, being rapidly metabolized to 13,14-dihydro-15-keto-PGF2a and that prostaglandins, at least in part, contribute to hypoxic pulmonary vasoconstriction.