Prostacyclin, thromboxane and antioxidant levels in pregnancy-induced hypertension

Abstract

1. Plasma 6-keto-prostaglandin F 1α (6-keto-PGF 1α, a major metabolite of prostacyclin), plasma thromboxane B 2 (TXB 2, a major metabolite of thromboxan A 2) and five antioxidants (indirect markers of reactive oxygen species) namely, plasma thiol, erythrocyte lysate thiol, erythrocyte superoxide dismutase, plasma total gluthathione and erythrocyte membrane thiol, were measured in 25 healthy non-pregnant women, 36 normotensive pregnant women and 35 women with pregnancy-induced hypertension (PIH). 2. The levels of TXB 2 were significantly increased in normal pregnant women and PIH women with or without proteinuria compared with non-pregnant women. The concentrations of TXB 2 in PIH women with proteinuria were higher than those without proteinuria ( P < 0.05). 3. The levels of 6-keto-PGF 1α in healthy non-pregnant women and PIH women with or without proteinuria were significantly lower than that in normotensive pregnant women (all of three P < 0.01). There were no significant differences between healthy non-pregnant women and PIH women with and without proteinuria. 4. The ratio of TXB 2 to 6-keto-PGF 1α was markedly elevated in PIH women with or without proteinuria compared with normotensive pregnant women and healthy non-pregnant women. The difference between PIH women with proteinuria and those without proteinuria was not significant ( P > 0.05). 5. The levels of plasma thiol, superoxide dismutase and glutathione were significantly decreased in PIH women compared with normotensive pregnant women. 6. There were significant positive correlations between the levels of prostaglandins and antioxidant activity. 7. These results demonstrate that there is an imbalance between TXB 2 and 6-keto-PGF 1α in women with PIH and decreased antioxidant levels which may reflect an increased activity of reactive oxygen species. The data suggest that the changes in the activity of reactive oxygen species may have a causative role in the abnormal pattern of TXA 2 and PGI 2 production in patients with PIH.