摘要
目的 建立诱导脑缺血耐受的缺血预处理模型并研究其对脑组织超氧化物歧化酶（ＳＯＤ）和谷胱甘肽过氧化物酶（ＧＳＨ－ＰＸ）活性的影响。方法 动物分别给予假预处理（ＳＨＡＭ），一侧颈内动脉注射生理盐水（ＳＩ）、双侧颈总动脉夹闭（ＢＣＡＯ）和双侧颈总动脉夹闭同时一侧颈内动脉注射生理盐水（ＢＳ），２４ｈ后腔内线栓法制作大脑中动脉阻断（ＭＣＡＯ）模型。观察ＭＣＡＯ后７２ｈ ４组脑梗死体积，观察各组预处理２４ｈ和 ＭＣＡＯ ２４ｈ、４８ｈ缺血侧脑组织ＳＯＤ和ＧＳＨ－ＰＸ活力。结果 ＢＳ组脑梗死体积明显低于其它３组（Ｐ＜０．０５）．预处理后２４ｈ ＢＳ组缺血侧脑组织ＳＯＤ和ＧＳＨ－ＰＸ活力明显高于其它组（Ｐ＜０．０１）；ＭＣＡＯ ２４ｈ、４８ｈ ４组缺血侧脑组织ＳＯＤ和ＧＳＨ－ＰＸ活力均明显降低，ＢＳ组ＳＯＤ和ＧＳＨ－ＰＸ活力明显高于其它３组（Ｐ＞０．０１）。结论 双侧颈总动脉夹闭同时一侧颈内动脉注射生理盐水能诱导缺血耐受，该缺血预处理增高脑组织抗氧化活力，可能是缺血耐受产生的机制之一。
Objective To establish ischemic preconditioning (IP) model of inducing cerebral ischemic toler- ance and observe the effect of the IP on SOD and GSH-PX activities of brain Methods Animals were given four different pretreatments 24h before MCAO: shamed operation(SHAM).onlv injected with saline into right internal carotid artery(SI), both carotid artery occlusion(BCAO) or given BCAO with SI(BS) simultaneously , focal cere- bral ischemia was made using the method of thread inserting right middle cerebral artery occlusion (MCAO). Cere- bral infarction volume was observed at 72h after MCAO. SOD and GSH-PX activities of ischemic hemisphere brains were observed at 24h after treatments and at 24h 、 48h after MCAO. Results Cerebral infarction volume was sig- nificantly decreased in BS group ( P <0. 05). SOD and GSH-PX activities of right brain were significantly in- creased in BS group at 24h after pretreatment( P <0. 01). SOD and GSH-PX activities of right brain were signifi- cantly decreased at 24h and at 48h after MCAO. Compared to other groups. SOD and GSH-PX activities in BS group were higher( P <0. 01). Conclusion BS pretreatment can induce cerebral ischemic tolerance. The ischemic preconditioning increases antioxidant activity of brain .which may take an important role in the mechanism of cere- bral ischemic tolerance.
出处
《中风与神经疾病杂志》
CAS
CSCD
北大核心
2001年第6期338-340,共3页
Journal of Apoplexy and Nervous Diseases
