Effect of amniotic fluid on platelet thromboxane production

We have studied the effect of amniotic fluid on thromboxane A2 (TXA2) production as an initial step in an evaluation of the role of this metabolite as the mediator of the pulmonary hypertension that accompanies perinatal aspiration. Term amniotic fluid enhanced platelet thromboxane B2 (TXB2) production in the presence of the aggregating agents thrombin and arachidonic acid, activity being confined to the lipid fraction. Compared with a baseline production of 1.4 +/- 0.45 pmol TXB2/10(6) platelets in response to thrombin (1 U/ml), unfractionated amniotic fluid or its lipid fraction enhanced TXB2 production to 2.87 +/- 0.53 and 2.81 +/- 0.62 pmol, respectively (P less than 0.01). Values for the aqueous extract were no different from buffer control values (1.14 +/- 0.5). No enhancement of platelet TXB2 production was observed in amniotic fluid obtained at 15 to 17 weeks. Similar activity was observed with either adult or neonatal platelets. This thromboxane enhancing property of amniotic fluid appears to be distinct from its thrombin generating property. Following perinatal aspiration, in situ production of thrombin and proaggregatory TXA2 could recruit more platelets, enhance local TXA2 production, and be responsible for the platelet thrombi that have been documented at autopsy in the pulmonary microcirculation in infants with perinatal aspiration syndrome.