The major cyclooxygenase metabolite of arachidonic acid (AA) in endothelial cells is prostacyclin (PGI2). Although most primary prostaglandins constrict the pulmonary vasculature, PGI2 is a pulmonary vasodilator. In the pulmonary circulation, optimal matching of blood flow to oxygenated alveoli is achieved by regulating the distribution of intrapulmonary blood flow. Alveoli exposed to reduced oxygen tension produce increases in pulmonary vascular resistance (PVR) resulting from hypoxic pulmonary vasoconstriction. These vasoconstrictor influences are opposed by endogenous vasodilator substances such as PGI2. It has previously been shown that exogenous administration of 5,6- epoxyeicosatrienoic acid (5,6-EET) into the intact canine pulmonary circulation opposes increases in PVR and results in large increases in PGI2 synthesis. Therefore it is proposed that stimulation by 5,6-EET in the pulmonary circulation results in increased synthesis of the pulmonary vasodilator, PGI2 which may mediate the vasodilator activity of 5,6-EET.
