Preeclampsia: a review of the role of prostaglandins.
The etiology of preeclampsia remains unknown. Because of their widespread and varied effects in the human body, prostaglandins--specifically PGI2, thromboxane A2, PGE, and PGF2 alpha--have come under much investigation as possible etiologic factors. The vasodilating, platelet-disaggregating prostaglandins (PGI2 and PGE) are increased during normal pregnancy and may account for many of the observed hemodynamic changes, which begin as early as the first trimester. In contrast, a relative increase in the vasoconstricting, platelet-aggregating prostaglandins (thromboxane A2 and PGF2 alpha) is seen in preeclampsia. The disruption in the delicate balance between these two opposing pairs of prostaglandins may play an important role in the causation of preeclampsia. The growing body of literature that deals with the relationship between prostaglandins and preeclampsia is discussed.
Friedman
S A
SA
Department of Gynecology and Obstetrics, Johns Hopkins Hospital, Baltimore, Maryland.
D015237:Dinoprost; D011464:Epoprostenol / Q000502:physiology; D005260:Female; D006801:Humans; D011225:Pre-Eclampsia / Q000503:physiopathology*; D011247:Pregnancy; D011453:Prostaglandins / Q000502:physiology*; D011458:Prostaglandins E / Q000502:physiology; D011460:Prostaglandins F / Q000502:physiology; D013928:Thromboxane A2 / Q000502:physiology
D011453:Prostaglandins; D011458:Prostaglandins E; D011460:Prostaglandins F; D013928:Thromboxane A2; D015237:Dinoprost; D011464:Epoprostenol