Hypertensive disorders in pregnancy. The role of eicosanoids.

Abstract

Pregnancies complicated by hypertensive disorders are always extremely hazardous for mother and child. In up to 30% of pregnant women this disease is characterized by feto-maternal dysfunction, looking like a kind of "chronic anaphylactoid reaction". As a result of defective genetic control, immunologic events seem to be the central etiologic aspect. Arteriolar vasospasm, pathology of platelets, disseminated intravascular coagulation and finally, elevation of maternal blood pressure, all these symptoms can be regarded as a reaction to immunologic processes. The central role of eicosanoids in the pathogenesis of pregnancy induced hypertension/preeclampsia-eclampsia is generally accepted. We can explain almost all known pathophysiologic abnormalities to be the consequence of disturbed eicosanoid production in a multitude of organs or organ systems. Defective placentation provokes poorly perfused placental tissue. This is correlated with endothelial cell disorder, endothelial damage and denudation. The resulting platelet activation, dysfunction of coagulation and vasoconstriction are due to an increased ratio between vasoconstricting and vasodilating eicosanoids. The suppression of prostacyclin (and PGE) formation in the fetal-placental-maternal unit even before the clinical manifestation of the disease seems to be the conditio sine qua non. So, the homeostatic response to the effects of vasoconstrictors (such as angiotensin, serotonin etc.) in the general and in the placental circulation is impaired. The depressed prostacyclin (and PGE) biosynthesis can be measured in urine. Altered urinary metabolite excretion appears to be a very early index for patients at risk to develop pregnancy-induced hypertension.