Nitric oxide and prostacyclin inhibit fetal platelet aggregation: a response similar to that observed in adults.

Abstract

We evaluated the relative importance of two endothelium-derived substances, prostacyclin and nitric oxide, in their ability to inhibit aggregation of fetal and maternal platelets. The effects of various concentrations of prostacyclin and S-nitroso-N-acetylpenicillamine (which releases nitric oxide) on platelet aggregation were studied by means of platelet-rich plasma from at least five to six subjects per group. Fetal blood was collected from umbilical vein at delivery. Maternal venous blood was collected within 4 hours of delivery. Platelet aggregation was monitored with a platelet aggregation profiler. Adenosine diphosphate was used as the aggregating agent. Statistical differences between means were evaluated with two-way analysis of variance or Student t test. Prostacyclin and S-nitroso-N-acetylpenicillamine inhibited aggregation of fetal and maternal platelets, but prostacyclin was more potent. Fetal platelets were more sensitive than maternal platelets to prostacyclin and S-nitroso-N-acetylpenicillamine. Prostacyclin appears to be more important in preventing aggregation of platelets in the feto placental circulation.