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40只家兔随机分为假手术组（A组）、缺血组（B组）、缺血再灌流组（C组）、治疗组（D组）。采用闭塞双侧颈总动脉和椎动脉及体循环低血压法建立急性完全性脑缺血再灌流损伤模型，缺血时限20min，再灌流2h，观察了脑组织Ca2＋、脂质过氧化产物一丙二醛（MDA）含量、超氧歧化酶（SOD）活性及脑组织超微结构改变。结果发现：治疗组于再灌流前1min注射山莨菪碱10mg／kg体重，并以5mg／h维持2h，脑组织Ca2＋、MDA含量较缺血组及缺血再灌流组明显降低，（P＜0．05，P＜0．01），SOD活性较缺血再灌流组明显增加（P＜0．05）同时脑组织超微结构损伤明显减轻。结果表明；再灌流早期给予山莨菪碱治疗对完全性脑缺血再灌注损伤具有明显保护作用。膜稳定作用、Ca2＋拮抗作用、抗脂质过氧化是其重要的作用环节。
Forty rabbits were randomly divided into sham operation group (A group), ischemia group (B group), ischemia reperfusion group (C group) and treatment group (D group). Acute complete cerebral ischemia-reperfusion injury model was established by occlusion of both common carotid artery and vertebral artery and systemic hypotension. The ischemic time was 20 min and reperfusion for 2 h. The effects of Ca2 +, lipid peroxidation product Aldehyde (MDA) content, superoxide dismutase (SOD) activity and ultrastructure of brain tissue. The results showed that in the treatment group, anisodamine 10 mg / kg body weight was injected 1 min before reperfusion and maintained at 5 mg / h for 2 h. The content of Ca2 + and MDA in brain tissue in the treatment group was significantly lower than that in the ischemia group and the ischemia-reperfusion group (P <0 .05, P <0.01). The SOD activity was significantly increased compared with the ischemia / reperfusion group (P <0.05). Meanwhile, the ultrastructural damage of brain tissue was significantly reduced. The results showed that the administration of anisodamine in the early period of reperfusion had a significant protective effect on complete cerebral ischemia-reperfusion injury. Membrane stability, Ca2 + antagonism, anti-lipid peroxidation is an important part of its role.