The role of eicosanoids and endothelium-dependent factors in regulation of the fetal pulmonary circulation.

Abstract

A complex interaction of mechanical, hormonal, vasoactive, morphological and gaseous factors is responsible for the transitional period and maintenance of these changes in the newborn period. Vasoactive eicosanoids, formed at multiple sites in the lungs exert multiple effects on the perinatal pulmonary circulation. By direct, as well as indirect interaction with other systems, eicosanoids appear to have a role in the rearrangement of the circulation at birth. At this time PGE1, acetylcholine, bradykinin, and endothelin appears to work, at least in part, to cause fetal pulmonary vasodilation via the release of EDRF. Products of the lipoxygenase pathway are powerful vasoconstrictors, but may not be important in regulation of high fetal pulmonary vascular tone or the pulmonary pressor response to hypoxia.