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

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 characterized by 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 women with 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 < 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.