CAJ | 학술논문

目的：探讨尼莫地平和东莨菪碱治疗脑缺血再灌注损伤的作用机理。方法：夹闭双侧颈总动脉和椎动脉复制脑完全性缺血模型。60只家兔均分成六组，假手术组、脑缺血组、脑缺血再灌注组、脑低温治疗组、东莨菪碱治疗组、尼莫地平治疗组。采集脑和血液标本测量Na+-K+-ATPase、超氧化物歧化酶（SOD）、丙二醛（MDA）活性。结果：缺血再灌注组脑组织SOD和Na+-K+-ATPase活性降低、MDA含量升高；相反，治疗组SOD和Na+-K+-ATPase活性升高，MDA含量降低。结论：东莨菪碱和尼莫地平具有保护缺血再灌注组脑组织Na+-K+-ATPase活性的作用，其机理可能与它们抑制自由基介导的脂质过氧化，减少脂质过氧化物的生成有关。
목적：탐토니막지평화동랑탕감치료뇌결혈재관주손상적작용궤리。방법：협폐쌍측경총동맥화추동맥복제뇌완전성결혈모형。60지가토균분성륙조，가수술조、뇌결혈조、뇌결혈재관주조、뇌저온치료조、동랑탕감치료조、니막지평치료조。채집뇌화혈액표본측량Na+-K+-ATPase、초양화물기화매（SOD）、병이철（MDA）활성。결과：결혈재관주조뇌조직SOD화Na+-K+-ATPase활성강저、MDA함량승고；상반，치료조SOD화Na+-K+-ATPase활성승고，MDA함량강저。결론：동랑탕감화니막지평구유보호결혈재관주조뇌조직Na+-K+-ATPase활성적작용，기궤리가능여타문억제자유기개도적지질과양화，감소지질과양화물적생성유관。
Objective: To discuss the effect and mechanics of scopolamine and nimodipine in treating encephalon ischemia-reperfusion injury.Method: The ischemia-reperfusion model was made by occluding the rabbits bilateral common carotid artery and vertebral artery. 30 rabbits were divided into normal group, ischemia group, ischemia-reperfusion group, hypothermia treatment group, scopolamine treatment group and nimodipine treatment group. Blood samples were collected for assay of superoxide dismutase(SOD), malonic dialdehyde(MDA) and Na+-K+-ATPase. Result: The SOD and Na+-K+-ATPase activities reduced and the MDA level increased significantly in ischemia-reperfusion group. Otherwise, the SOD and Na+-K+-ATPase activities increased and the MDA level decreased in treatment group.Conclusion: Like the low temperature treatment, scopolamine and nimodipine can effectively protect the Na+-K+-ATPase activity in encephalon ischemia-reperfusion injury by inhibiting the reperfusion injury resulting from lipid peroxidation led by free radical.