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Introduction Since the identification of prostacyclin (PGI2) and thromboxane (TxA2) in the seventies [13] there is clear evidence that prostanoids play an important role in the regulation of the circulation. PGI2 is mainly synthesised in the endothelium and in the smooth muscles of the vascular wall and is one of the strongest dilatatory substances in arteries, veins and capillaries. PGI2 causes a significant decrease in blood pressure [13, 23] and is a very potent inhibitor of the aggregation of thrombocytes. Thus, it is an antagonist of thromboxane (TxA2), which is produced in the thrombocytes and has a strong constrictor effect on blood vessels. Besides, PGI2 has an anti-arteriosclerotic effect by direct stimulation of cholesterol catabolism, leading to a release of cholesterol from the vascular wall, which is then removed by HDL proteins [17]. Furthermore, PGI2 is considered to have a cytoprotective function [17]. PGI2 is not stable in aqueous solution at physiological pH. However, 6-keto-prostaglandin Flct, which results from non-enzymatic hydrolysis, serves as a stable marker in plasma, urine and amniotic fluid [21]. TxA2 has a very short halftime too and only its stable metabolite TxB2 is a good marker. The importance of PGI2 and TxA2 for utero-placental
Journal of Perinatal Medicine – de Gruyter
Published: Jan 1, 1993
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