Roles of Thromboxane A₂ On High Salt Induced-Fetal Defect.

Preeclampsia is a pregnancy-induced disorder. If a pregnant woman suffered from preeclampsia, her worse developed-placenta might result in growth retardation of the fetus, and in the most severe cases, it would cause fetal and maternal death. Several previous studies showed that circulating thromboxane A₂ in preeclampsic women was higher than that of normal pregnant women, and higher thromboxane A₂ level might induce thrombosis and hypertension in these patients. Thus, thromboxane A₂ was thought to be an important metabolite relevant to the development of preeclampsia.

In order to clearly clarify the roles of thromboxane A₂ on preeclampsia, wild type and thromboxane A₂ synthase knockout pregnant mice were fed with drinking water containing high concentration of sodium chloride. The effect of thromboxane A₂ on preeclampsia was observed by measuring blood pressure, urinary protein, systemic edema in pregnant mice, and placenta weight, fetal weight, fetal size and fetal sections were also measured and stained.

In the groups of pregnant mice fed with high salt, maternal body weight, fetal size and fetal weight were severely decreased in wild type mice as compared to thromboxane A₂ synthase knockout mice. Furthermore, abnormal cell degeneration was observed in fetus of wild type pregnant mice, but less in thromboxane A₂ synthase knockout fetus.

These results demonstrate that knockout pregnant mice were more resistant to high salt treatment, implying the roles of thromboxane A₂ on the development of maternal and fetal defects during high salt treatment.

No relevant conflicts of interest to declare.