The role of lipoxygenase and cyclooxygenase metabolites in acute hypoxic pulmonary vasoconstriction (HPV) was studied in piglets. It has been found that acute alveolar hypoxia induced remarkable pulmonary vasoconstriction, associated with an increase in cardiac output. The hypoxic pulmonary vasoconstriction response was insignificantly attenuated after infusion of DEC. Indomethacin potentiated markedly the increase in pulmonary artery pressure and pulmonary vascular resistance and thus augmented HPV. It is inferred that hypoxic pulmonary vasoconstriction in piglet may be mediated by other important mediators in addition to leukotrienes, but modulated by prostaglandins to prevent an excessive rise in pulmonary artery pressure.

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