Effects of trapidil on the PGI2 and TXA2 synthesis in human umbilical veins perfused in vitro.

Current therapeutical concepts for prophylactic treatment of preeclampsia are based on the hypothesis that this pathological state is mainly due to a functional imbalance between vascular prostacyclin (PGI2) and thromboxane A2 (TXA2) biosynthesis. The influence of Trapidil on PGI2 and TXA2 formation was studied by in vitro perfusion of human umbilical veins by measuring the production of the metabolites 6-keto-PGF1 alpha and TXB2, respectively, in the perfusates using Enzyme-Immunoassay. The basal production of 6-keto-PGF1 alpha was 90.6 pg/mL/cm of vessel wall, whereas TXB2 formation attained a rate of 7.5 pg/mL/cm. The addition of Trapidil to the perfusate resulted in a significant stimulation of PGI2 production but apparently does not exhibit any effect on TXB2 generation. These data support the suggestion that Trapidil may act by increasing the ratio of PGI2/TXA2 in favor of the antiaggregatory/vasodilatory PGI2.