The effect of acute hypoxia on prostaglandin release in perfused human fetal placenta.

The release of prostaglandin E2 and F2 alpha, thromboxane B2 and 6-keto-prostaglandin F1 alpha was measured in isolated human placental cotyledons perfused under high- and low-oxygen conditions. Also the effect of reoxygenation on prostaglandin production was studied. During the high-oxygen period, prostaglandin E2 accounted for 44% and 6-keto-prostaglandin F1 alpha for 28% of all prostaglandin release, and the rank order of prostaglandin release was E2 greater than 6-keto-prostaglandin F1 alpha greater than thromboxane B2 greater than prostaglandin F2 alpha. Hypoxia had no significant effect on quantitative prostaglandin release, but the ratio of prostaglandin E2 to prostaglandin F2 alpha was significantly increased. After the hypoxic period during reoxygenation the release of 6-keto-prostaglandin F1 alpha was significantly decreased, as was the ratio of 6-keto-prostaglandin F1 alpha to thromboxane B2. Also the ratio of the vasodilating prostaglandins (E2, 6-keto-prostaglandin F1 alpha) to the vasoconstricting prostaglandins (thromboxane B2, prostaglandin F2 alpha) was decreased during reoxygenation period. With the constant flow rate, the perfusion pressure increased during hypoxia in six and was unchanged in three preparations. The results indicate that changes in the tissue oxygenation in the placenta affect prostaglandin release in the fetal placental circulation. This may also have circulatory consequences.