活血化瘀中药对内毒素性休克内皮细胞的保护作用

目的 :探讨活血化瘀中药对内毒素性休克大鼠肺微血管内皮细胞的保护作用。方法 :选 Wistar大鼠 ,随机平分为对照组、模型组 (L PS)、地塞米松治疗组 (Dex)和活血化瘀中药治疗组 (AMRS)。电镜观察内皮细胞的超微结构改变 ,用电脑图像分析系统进行形态计测及肺微血管通透性指数 (PMPI)和循环内皮细胞 (CEC)数量的测定。结果 :AMRS组与 L PS组比较内皮细胞厚度极明显减小 (P<0 .0 0 1) ,胞饮泡体密度、细胞表面破损线密度、PMPI及 CEC数量均有明显差异 (P<0 .0 1或 P<0 .0 5 )。 AMRS组与 Dex组比 ,上述大多数指标有显著差异 (P均 <0 .0 5 ) ,微血管内血小板聚集、纤维素沉着和白细胞粘附内皮细胞现象也明显减少。结论 :在内毒素性休克中 ,活血化瘀中药在超微结构水平上能够改善、修复受损的内皮细胞 ,证实对内皮细胞具有保护作用

Protective effect of activating microcirculation and removing stasis medicinal herbs on the endothelial cells in endotoxin shock

Objective:To study protective effect of activating microcirculation and removing stasis medicinal herbs in the microvascular endothelial cells of lung in endotoxin shock.Methods:Wistar rats were divided randomly into four groups:control group (NS),endotoxin shock group (LPS),dexamethasone treatment group (Dex),and activating microcirculation and removing stasis medicinal herbs treatment group (AMRS).Electron microscope and computerized image analysis system were used to assess the ultrastructural lesion of microvascular endothelial cells of lung,quantitatively.The pulmonary microvascular permeability index (PMPI) and circulating endothelial cells (CEC) were measured respectively.Results:In comparison between AMRS and LPS group the thickness of endothelial was significantly reduced ( P <0 001).AMRS group compared with LPS group disclosed very significant or significant differences in the pinocytotic vasicles volume density (VD),the destructive length density (LD) on cell surface,PMPI,and the amount of CEC ( P <0 01 or P <0 05).In AMRS group compared with Dex group there were differences in most abovementioned indexes (all P <0 05),meanwhile the platelets aggregations,fibrin depositions and adherences of neutrophils on endothelial cells within the microvascular lumens,and all of the changes were greatly decreased.Conclusions:Ultrastructurally,AMRS appears to be able to improve and heal the damaged endothelial cells,so that is possesses the protective effects on endothelial cells in endotoxin shock.