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作 者:高鹏[1] 熊利泽[1] 路志红[1] 李万鹏 孟静茹[3]
机构地区:[1]第四军医大学西京医院麻醉科 [2]渭南市人民医院麻醉科,陕西渭南714000 [3]第四军医大学基础部药理学教研室,陕西西安710033
出 处:《第四军医大学学报》2006年第14期1273-1275,共3页Journal of the Fourth Military Medical University
基 金:国家自然科学基金(30471664)
摘 要:目的:通过在体兔脊髓缺血再灌注模型研究缺血后处理对兔脊髓缺血再灌注损伤后体内丙二醛(MDA)含量、超氧化物歧化酶(SOD)活性的影响.方法:雄性新西兰大白兔24只,随机分为4组,每组6只.对照组仅行单纯缺血再灌注处理;缺血后处理15s,30s和60s(PA,PB和PC)组分别于阻闭腹主动脉15min后,再灌注15s,30s和60s,缺血15s,30s和60s,反复3次.各组均在缺血前、缺血10min和再灌注1h时对所有动物抽动脉血并取脊髓组织匀浆后分别测定MDA含量和SOD活性.结果:再灌注1h时血浆和脊髓组织中MDA含量:PA和PB组明显低于对照组(P<0.01),而PC组明显高于对照组(P<0.01);SOD活性:PA和PB组明显高于对照组(P<0.01),PC组明显低于对照组(P<0.01).结论:早期短时程缺血后处理(15s/15s和30s/30s)具有抗氧化作用,能够抑制再灌注后氧自由基的过量生成,对兔脊髓缺血再灌注损伤具有一定保护作用.AIM: To investigate the impact of postischemic treatmem on malondialdehyde (MDA) and superoxide dismutase (SOD) during spinal cord ischemia/reperfusion injury in rabbits. METHODS: Twenty-four male New Zealand rabbits were randomly divided into 4 groups (n = 6 each ): control group, postischemic treatment for 15, 30 and 60 s groups ( PA, PB and PC groups). Rabbits in the control group underwent the occlusion of abdominal aorta for 15 rain followed by reperfusion for 1 h. In PA, PB and PC groups, rabbits underwent the 3 cycles of ischemia/reperfusion with the duration of 15 s/15 s, 30 s/30 s and 60 s/60 s respectively just after 15 min occlusion of the abdominal aorta. The MDA and SOD were measured at the 3 different time points :pre-ischemia, 10 min after ischemia and 1 h after reperfusion. RESULTS: At 1 h after reperfusion, the MDA concentrations in plasma and spinal cord homogenate in PA and PB groups were significantly lower than those in the control group (P 〈 0.01 ), but in PC group they were significantly higher than those in the control group ( P 〈 0.01 ). The SOD activities in plasma and spinal cord homogenate in PA and PB groups were significantly higher than those in the control group ( P 〈 0.01 ), while in PC group they were both significantly lower than those in the control group (P 〈 0. 01 ). CONCLUSION: Early and short-term ( 15 s/15 s and 30 s/30 s) ischemic postconditioning has an antioxidant potential, and depresses the production of oxygen free radicals and protects the spinal cord from ischemia/reperfusion injury.
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