Low-dose aspirin inhibits thromboxane, but not prostacyclin, production by human placental arteries.

Preeclampsia is associated with increased thromboxane and decreased prostacyclin production by the placenta. Low-dose aspirin can selectively inhibit thromboxane production in the adult circulation, but its effects on placental vascular production of thromboxane and prostacyclin are incompletely understood. We therefore studied the effects of low-dose aspirin on the production rates of prostacyclin and thromboxane, with and without vasoconstricting doses of angiotensin II, in human placental arteries. Chorionic plate arteries were incubated and samples were assayed for thromboxane and prostacyclin by radioimmunoassay of their stable metabolites. Production rates for prostacyclin were similar in the control, aspirin, angiotensin II, and angiotensin II plus aspirin groups. Mean (+/- SEM; n = 8) thromboxane production rates in the aspirin (1.4 +/- 0.5 pg/mg/hr) and angiotensin II plus aspirin (2.9 +/- 0.6 pg/mg/hr) groups were significantly lower (p less than 0.05) than values in the control (8.6 +/- 2.7 pg/mg/hr) and angiotensin II (6.7 +/- 1.3 pg/mg/hr) groups. We conclude that low-dose aspirin significantly decreases production of thromboxane in placental arteries both with and without vasoconstricting doses of angiotensin II.