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In normal pregnancy platelet aggregation and blood flow in the uterine arteries could be modulated by the balance between the prostacyclin-generating system in the uterine arterial walls and the thromboxane-generating system in platelets. Since hypertensive pregnancies and pregnancies complicated by insufficient fetal growth are characterizedby a diminished uteroplacental blood flow,the present study was performed to investigate platelet thromboxane synthesis in these conditions.  Material and methods. The study was performed in a control group of 27 women with uncomplicated pregnancies and adequate-for-gestational age (AGA)infants(group I),23 women with uncomplicated pregnancies but small-for-gestational age(SGA) infants(group II); 18 women with pregnancy-induced hypertension (PIH) and AGA-infants(group III); 16 womenwith PIH and SGA infants(group V).All women were investigated in the last trimester of pregnancy. Venous blood was obtained in EDTA. Platelet aggregation was induced with thrombin( l I.U./ml final concentration)in platelet-rich plasma, and the amount of malondehyde(MDA)generated was measured spectrophotometrically after reaction with thiobarbituric acid. The amount of MDA is equivalent to that of HHT and a measure of the formation of thromboxane.  Results. The amount of MDA (mmol/109 platelets ± S.D.)formed in group I was 5.35±0.8, in group II 6.32± 1.4,in group III 6.3 ± 1.5, and in group IV 6.4 ± 1.8. Groups II, III and IV were not different from each other, but were all significantly higher than group I(p &lt; 0.01).  Conclusion. The results indicate that pregnant women with a high incidence of a compromised uterine circulation-normotensive with SGA, hypertensive with AGA or SGA- as a group exhibit a more active platelet thromboxane-synthesis. This might be due to defective production of PGI2 by the uterine arterial wall.

Enhanced Platelet Thromboxane Synthesis In Normotensive And Hypertensive Pregnancies With Insufficient Fetal Growth