Xu S
Institute of Basic Medical Sciences, Beijing.
Zhongguo Yi Xue Ke Xue Yuan Xue Bao. 1990 Aug;12(4):306-10.
Bacterial endotoxin binds to platelets and causes platelet aggregation, thrombocytopenia, increase in thromboxane A2 production, serotonin release and increase in the generation of platelet factor 3 procoagulant activity. These effects have been demonstrated in a variety of animal species. Much evidence has shown that such changes may participate in the pathogenesis of DIC and RDS in septic shock. The anisodamine (654) antishock effect has been studied from different angles for more than 20 years, with its effect on the cardiovascular system, including the microcirculation, being demonstrated. But few reports concerning its effect on platelet function have emerged. In this study, the effect of anisodamine on rabbit platelet aggregation, release, morphological changes, cellular cAMP, and membrane lipid fluidity induced by E. coli endotoxin were studied both in vivo and in vitro. After anisodamine intervention, all of these parameters improved to a certain extent. The possible protective mechanisms of anisodamine on platelets both in vivo and in vitro are discussed.
细菌内毒素与血小板结合，导致血小板聚集、血小板减少、血栓素A2生成增加、5-羟色胺释放以及血小板因子3促凝活性生成增加。这些效应已在多种动物物种中得到证实。大量证据表明，此类变化可能参与脓毒性休克中弥散性血管内凝血（DIC）和呼吸窘迫综合征（RDS）的发病机制。山莨菪碱（654）的抗休克作用已从不同角度研究了20多年，其对心血管系统（包括微循环）的作用已得到证实。但关于其对血小板功能影响的报道却很少。在本研究中，在体内和体外研究了山莨菪碱对大肠杆菌内毒素诱导的兔血小板聚集、释放、形态变化、细胞环磷酸腺苷（cAMP）和膜脂流动性的影响。山莨菪碱干预后，所有这些参数均有一定程度的改善。并讨论了山莨菪碱在体内和体外对血小板可能的保护机制。
