Platelet prostacyclin receptors in myocardial infarction

在动脉血栓形成的发展过程中，如心肌梗死或脑血栓形成，血小板被认为起着重要作用。前列环素(PGI_2)是由内皮细胞中的前列环素合成酶合成的，通过升高血小板环磷酸腺苷(CAMP)和阻断钙动员来抑制血小板功能。在动脉血栓多发的高脂血症患者中，用稳定的前列腺素I_2类似物伊洛前列素研究其与血小板的相互作用是值得研究的。高脂血症患者28例，其中IIa型14例，IIb型10例，IV型4例。IIa型和IIb型患者的血小板中可引起50%抑制胶原诱导的血小板聚集的PGI_2浓度(10mug/ml胶原)显著低于对照组。IIa型和IIb型患者血小板膜上[H^3N-iloprost]结合位点数明显高于对照组。反之，经PGI_2和IBMX孵育后，高脂血症患者的血小板cAMP浓度升高幅度较小，提示高脂血症患者的血小板信号转导可能存在异常。然而，PGI_2对这些血小板作用的详细机制尚需进一步研究。

In the development of arterial thrombosis such as myocardial infarction or cerebral thrombosis, blood platelets are believed to play a major role. Prostacyclin (PGI_2) is synthesized by the action of prostacyclin synthetase in endothelial cells and inhibits platelet functions via its ability to elevate platelet cyclic AMP(cAMP) and block calcium mobilization. It is therfore worthwhile to study interaction between platelets and PGI_2 by using Iloprost, a stable PGI 1 analogue, in patients with hyperlipidemia in that arterial thromboses are frequently encountered.Twentyeight patients with hyperllipidemia including 14 patients with type II a, 10 with type II b and 4 with type IV were involved in this study.Concentrations of PGI_2 which can cause 50% inhibition of collagen-induced platelet aggregation (10mug/ml collagen) were significantly lower in platelets from patients with type II a and type II b than control. Number of binding sites of [H^3N-Iloprost on platelet membranes was found to be higher in patients with type II a and type II b than control group. On the contraly, platelet cAMP concentrations, measured by ELISA, elevated less in platelets from hyperlipidemic patients after incubation with PGI_2 and IBMX, a potent phosphodieste-rase inhibitor.From these results it is suggested that there might be some abnormalities in signal transduction in platelets from hyperlipidemic patients. However, further studies are necessary to elucidate the detailed mechanism of PGI_2 action on those platelets.