Platelet prostacyclin receptors in myocardial infarction

在动脉血栓形成如心肌梗塞或脑血栓形成的发展中，血小板被认为起主要作用。前列环素（prostacyclin，PGI_2）是由内皮细胞合成的前列环素合成酶（prostacyclinsynthetase，PGI_2），通过升高血小板环磷酸腺苷（cyclicAMP，cAMP）和阻断钙动员而抑制血小板功能。高脂血症是动脉血栓形成的主要原因，研究血小板与PGI_2的相互作用是值得的。28例高脂血症患者，其中Ⅱ a型14例，Ⅱ型B型10例，Ⅳ型4例，测定了对胶原诱导的血小板聚集有50%抑制作用的PGI_2浓度Ⅱ a型和Ⅱ B型患者血小板中的胶原蛋白（10 μ g/ml）显著低于对照组。Ⅱ a型和Ⅱ B型患者血小板膜上[H ^3 N]-伊洛前列素结合位点数均高于对照组。而用酶联免疫吸附法测定的高脂血症患者血小板中cAMP浓度，经PGI_2和磷酸二酯酶抑制剂IBMX孵育后升高幅度较小，提示高脂血症患者血小板中可能存在某些信号转导异常。但PGI_2对血小板的作用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.