Postnatal regulation of the pulmonary circulation: a role for lipid mediators?

The action and interaction of many products of arachidonic acid metabolism can affect the pulmonary circulation in the perinatal period. The rapid increase in pulmonary blood flow with the onset of ventilation likely is brought about to a large degree by the production locally of prostaglandin I2 (PGI2). This can be stimulated by purely mechanical factors, by the normally increasing concentrations of angiotension II, by the 02-mediated release of bradykinin, or perhaps by other phenomena. Prostaglandin D2 release from mast cells also may play some role. The opposing pulmonary vascular effect, i.e., pulmonary vasoconstriction, of leukotrienes is likely to play a role in regulating fetal pulmonary blood flow. Inhibition of the production or action of these substances will allow for vasodilatation, and it is probable that perinatal pulmonary vascular tone reflects a balance between local prostaglandin and leukotriene production.