| Summary: | 碩士 === 台北醫學院 === 醫學研究所 === 88 === Abstract
There are considerable evidences of platelet hyperaggregability in women during pregnancy in vivo. This may contribute to the hypercoagulation which occurs during pregnancy which may in turn play an important role in thromboembolism and disseminated intravascular coagulation.
Previous studies suggest that platelets from pregnancy women increased sensitivity to aggregating agonists via a thromboxane-dependent manner.
In this study, we found that platelet aggregation was significantly increased induced by ADP (20 mM), collagen (1 mg/ml) and thrombin (0.04 U/ml) in healthy pregnant platelet suspensions as compared with non-pregnant platelets. This may imply that pregnant platelets potentiate fibrinogen binding to fibrinogen receptor associated with the glycoproetin IIb/IIIa complex. However, we found that pregnant platelet suspensions did not significantly affect the FITC-triflavin binding to the glycoprotein IIb/IIIa complex.
In addition, collagen (10 mg/ml) induced intracellular [Ca2+] mobilization of pregnant platelets were markedly higher than non-pregnant platelets. Furthermore, our results also revealed that the levels of thromboxane A2 formation induced by collagen (4 mg/ml) in pregnant platelets were higher than non-pregnant platelets. In addition, we found that levels of prostaglandin E2 formation induced by arachidonic acid (100mM) in pregnant platelets did not differ from the non-pregnant platelets. On the other hand, we also found that the levels of cyclic AMP in pregnant platelets were less than non-pregnant platelets. By means of imidazole (600 mM) and indomethacin (500 mM) to inhibit thromboxane A2 synthesis, the levels of cyclic AMP both in pregnant and non-pregnant platelet suspensions were not significantly difference. Furthermore, thrombin-induced intracellular DpH change was markedly in pregnant platelets. It implies that inhibition of cyclic AMP may promote the Na+/H+ changer in human platelets. In contrast, the nitrate formation was not significantly different between pregnant and non-pregnant platelets.
These results indicate that the phenomenon of platelet hyperaggregability in pregnant platelets may initially induce the thromboxane A2 formation, resulting in inhibition of platelet membrane-associated adenylate cyclase, thereby lowering the cyclic AMP levels in platelets, followed by the increase of intracellular DpH, finally elevated the intracellular Ca2+ mobilization.
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