Platelet prostacyclin receptors in myocardial infarction

在动脉血栓形成，如心肌梗死或脑血栓形成的发展中，血小板被认为发挥了重要作用。前列环素（PGI_2）是由前列环素合成酶在内皮细胞中合成的，通过提高血小板环AMP（cAMP）和阻断钙动员来抑制血小板功能。因此，在经常发生动脉血栓形成的高脂血症患者中，使用伊洛前列素（一种稳定的pgi1类似物）来研究血小板与pgi2之间的相互作用是值得的。本研究共纳入28例高脂血症患者，其中ⅱa型14例，ⅱb型10例，ⅳ型4例。对胶原诱导的血小板聚集有50%抑制作用的PGI_2浓度（10mug/ml胶原）在ⅱa型和ⅱb型患者的血小板中显著低于对照组。ⅱa型和ⅱb型患者血小板膜上[H^3N-Iloprost结合位点数量均高于对照组。相反，ELISA测定的血小板cAMP浓度在PGI_2和IBMX（一种有效的磷酸二酯酶抑制剂）孵育后，在高脂血症患者的血小板中升高较少。这些结果提示，高脂血症患者血小板信号转导可能存在一些异常。然而，PGI_2作用于这些血小板的具体机制还有待进一步研究。

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.