Laffi G, Cominelli F, Ruggiero M, Fedi S, Chiarugi V, Gentilini P
FEBS Lett. 1987 Aug 10;220(1):217-9. doi: 10.1016/0014-5793(87)80907-9.
We have studied platelet function in 10 patients with severe liver cirrhosis, compared to healthy subjects. Using washed platelets, we have investigated the molecular mechanism underlying the defect in platelet aggregation frequently observed in these patients. We have found that platelets from cirrhotic patients have a reduced responsiveness to thrombin and collagen in terms of aggregation, and receptor-dependent activation of phospholipase C, A2 and cyclooxygenase/thromboxane synthetase. We thus suggest that this impairment in transmembrane signalling is responsible for the defective platelet function observed in cirrhosis.
我们研究了10例严重肝硬化患者的血小板功能，并与健康受试者进行了比较。我们使用洗涤过的血小板，研究了这些患者中经常观察到的血小板聚集缺陷背后的分子机制。我们发现，肝硬化患者的血小板在聚集、磷脂酶C、A2以及环氧化酶/血栓素合成酶的受体依赖性激活方面，对凝血酶和胶原蛋白的反应性降低。因此，我们认为这种跨膜信号传导的损害是肝硬化中观察到的血小板功能缺陷的原因。
