Summary
There is substantial evidence of increased platelet reactivity in vivo and in vitro
during pregnancy. Previous in vitro studies suggest that platelets from pregnant women
show increased sensitivity to agonists, the response to which has a thromboxane dependent
component. The aim of this study was to determine whether this is due to increased
activity of the thromboxane biosynthetic pathway or to increased platelet sensitivity
to the effects of thromboxane. During pregnancy, platelets were more sensitive to
the pro-aggregatory effects in vitro of the thromboxane mimetic U46619, in whole blood
and in platelet rich plasma, compared to those from non-pregnant controls. The difference
in extent of U46619-induced platelet aggregation between groups was abolished in the
presence of a high concentration of the specific thromboxane antagonist ICI 192605,
but not by prior incubation of blood with aspirin. Platelets from pregnant women were
significantly less sensitive to inhibition of arachidonic acid induced activation
by the thromboxane synthetase inhibitor dazmegrel, but there was no change in platelet
cyclic AMP accumulation under these conditions. Arachidonic acid induced platelet
thromboxane B2 production was similar in pregnant and non-pregnant subjects. In conclusion,
platelets are more sensitive to the activating effects of thromboxane during pregnancy,
but there is no change in the intrinsic reactivity of the thromboxane biosynthetic
pathway.