摘要
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。
The modle of complete cerebral ischemla was induced by ligation of bi1ateral common carotids and vertebral arteries with systemic hypotension followed by reperfusion. Forty rabbits were randomly divided into four groups. Sham group (group A)undergoing all surgical precedures but ischemia. Ischemic group (group B) undergoing global brain ischemia for twenty minutes, ischemia-reperfusion group (group C) suffering from g1obal brain ischemia for twenty minutes and reperfusion for two hours, and treated group (group D) receiving intravenous infusio n of anisodamine 10mg/kg body weght at one minute be fore reperfusion after suffering from brain ischemia and injection lasting for two hours at 5mg/h. After conipleting the required precedures, the samples of brain tissues were taken to measure the contents of calcium, lipid peroxide malondiadhyde (MDA), the activity of superoxide dismutase (SOD), and to observe the ultrastructure of cortex. The results showed that the levels of calcium, MDA in group D were reduced significantly in camparison with those in the group B, C (P<0. 05, P<0. 01), the activity of SOD was increased markedly (P<0. 05 vs group C) the brain ultrastructural damages were attenuated apparently. The results suggested that anisodamine have a remarkable protection against the damage by ischemia and reperfusion. Its mechanisms of protection on the damage may be involved in stablization of membranes, antagonism of calcium, and inhibition of lipid peroxidation.
出处
《急诊医学》
CSCD
1998年第1期32-34,共3页
