Abstract
Current therapeutical concepts for prophylactic treatment of pre-eclampsia are based on the hypothesis that this pathological state is mainly due to a functional imbalance between vascular prostacyclin (PGI 2) and thromboxane A 2 (TXA 2) biosynthesis. The influence of Trapidil on PGI 2 and TXA 2 formation was studied by in vitro perfusion of human umbilical veins by measuring the production of the metabolites 6-keto-PGF 1α and TXB 2, respectively, in the perfusates using Enzyme-Immunoassay. The basal production of 6-keto-PGF 1α was 90.6 pg/mL/cm of vessel wall, whereas TXB 2 formation attained a rate of 7.5 pg/mL/cm. The addition of Trapidil to the perfusate resulted in a significant stimulation of PGI 2 production but apparently does not exhibit any effect on TXB 2 generation. These data support the suggestion that Trapidil may act by increasing the ratio of PGI 2/TXA 2 in favor of the antiaggregatory/vasodilatory PGI 2.
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