中文摘要：

目的研究肾上腺素能否直接损伤血管内皮细胞（VEC），引起血栓形成，为今后研究肾上腺素过度脱氨损伤VEC机制研究和研发特异性防护药物打下基础。方法将家兔分成3组，肾上腺素组、生理盐水组和依诺肝素组。通过插管于股动脉游离段分别注入肾上腺素-生理盐水液、生理盐水，依诺肝素-肾上腺素液，保留25min后，动脉插管连接生物信号记录系统，观察血压曲线，当曲线变为直线即为血栓堵塞形成，记录栓塞时间。取与药物接触的股动脉段做切片，观察血管内皮的病理变化。结果肾上腺素组（20．08±1．72）min的栓塞时间显著短于生理盐水组（56．55±4．39）min和依诺肝素组（53．73±5．06）min（P〈0．01），生理盐水组栓塞时间与依诺肝素组无明显差别。形态学观察股动脉血管显示，生理盐水组内皮质完整、光滑；肾上腺素组断裂、脱落较严重；依诺肝素组较完整，局部表面粗糙。结论肾上腺素能够直接损伤VEC，导致动脉血栓形成。

英文摘要：

Objective To study whether adrenaline injure vascular endothelial cell （VEC） directly to cause thrombosis and erect a foundation for the mechanism reaserch of VEC damage caused by adrenergic excessive deamination and the research of specific protection drug. Methods rabbits were divided into three groups： adrenalin group, saline group and enoxaparin group. Adrenalin-saline, saline and enoxaparin-saline were injected into the dissociated femoral via a cannula and keep for 25 minutes. Then, the arterial cannula was connected with a biological message recorder to show arterial pressure. The change of pressure curve to baseline presented the formation of thrombotic occlusion.The occlusion time was recorded.The pathological changes of the vascular endothelium on femoral sections contacted with adrenaline were observed.Results The occlusion time of adrenalin group （20.08 ± 1.72 min ） was short significantly than that of saline group （56.55 ± 4.39 min ）and enoxaparin group （ 53.73± 5.06 min） （P〈0.01）. There was no statistical significances on occlusion time between saline group and enoxaparin group.The morphologic observation of femoral displayed that the endothelium was intact and smooth in saline, endothelium ruptures and breaks off in adrenaline, and coarse surface appears but not breaks off in enoxaparin group.Conchltsion Adrenline can damage VEC and diroetly cause arterial thrombosis.