Platelet Function in Normal Pregnancy

The concept for this thesis arose after a collaboration between the Platelet Biology Laboratory and the Department of Obstetrics and Gyanecology in the Royal College of Surgeons in Ireland. They discovered a significant difference in platelet aggregation in women with a history of recurrent pregnancy loss using a novel platelet assay. This posed the question as to whether or not this platelet assay would eludicate different platelet reactivity at different time points in a normal, heathy pregnancy. The objective was to critically evaluate platelet reactivity in normal pregnancy using this assay which assessed platelet aggregation to several agonists at multiple submaximal doses using a modification of light transmission aggregometry. Two groups of women were examined in the study; a non-pregnant control group and pregnant women assessed longitudinally in normal pregnancy and in the postnatal period. There are two main findings in this thesis. Firstly, in the first trimester of pregnancy there is a reduction in platelet reactivity compared to the non-pregnant controls in response to collagen, epinephrine and also seen with spontaneous platelet aggregation. Secondly, there was an increase in platelet reactivity in the second and third trimesters of pregnancy in relation to the agonist arachidonic acid. There are a number of potential hypotheses which may explain these findings. Matrix metalloproteinases, prostacyclin, female sex steroids, intrinsic inhibitors of platelets and other coagulation factors are explored in this thesis to identify their hypothetical role in influencing platelet function in pregnancy.