升高血压对大鼠脑缺血保护作用机制的研究  

The study of the protective mechanism of induced hypertension on cerebral ischem ia in rats

作　　者：矫黎东[1] 贾建平[1] 周冀英[1] 赵洪波[2] 

机构地区：[1]首都医科大学宣武医院神经内科,北京100053 [2]北京大学医学部药理室

出　　处：《中国脑血管病杂志》2005年第2期77-79,81,共4页Chinese Journal of Cerebrovascular Diseases

基　　金：国家自然科学基金资助项目 ( 3 0 3 70 493 )

摘　　要：目的　初步探讨升高血压对急性期脑梗死大鼠脑缺血损伤保护作用的机制。　方法　健康成年雄性SD大鼠 4 2只 ,随机分为 3组 ,正常对照组 (6只大鼠 )、升压治疗组 (采用改良线栓法分别阻塞大鼠大脑中动脉 3h、 4h和 6h制作梗死模型 ,分为H3 、H4、H63个亚组 ,每个亚组 6只大鼠 )和单纯缺血组 (I3 、I4、I63个亚组 ,每个亚组 6只大鼠 )。升压治疗组在缺血最后 1h用去氧肾上腺素 (苯肾上腺素 )升高系统血压 30 % ,正常对照组和单纯缺血组以等渗盐水作对照。用分光光度法测定大鼠脑组织匀浆中丙二醛含量及超氧化物歧化酶 (SOD)活性。　结果　脑缺血后各组大鼠脑组织丙二醛含量较正常对照组均有明显增加 (P <0 0 5 ) ,而且随缺血时间延长丙二醛含量增加明显 ;升压治疗后 ,丙二醛含量较单纯缺血组有不同程度的减少 ,H3 亚组丙二醛含量较I3 亚组差异有显著意义 (P <0 0 5 )。脑缺血后各组大鼠脑组织SOD活性均较正常对照组明显下降 (P <0 0 5 ) ,随时间延长SOD活性下降更加明显 ;升高血压治疗后SOD活性较单纯缺血组有不同程度的增加 ,其中H3 和H4组SOD活性的恢复差异有显著意义 (P <0 0 5 )。　结论　恢复脑组织SOD活性。ObjectiveTo study the protective mechanism of in duced hypertension for treating rat cerebral ischemia in the acute phase. Methods Forty-two adult Sprague-Dawley rats were randomly divided into three groups,that was control group、simple ischemic groups(I 3、I 4、I 6 subgroup) and induced hypertension groups(H 3、H 4、H 6 subgroup). The middle cerebral arteries were occluded(MCAO)with threads according to modified m ethod by 3 h、4 h and 6 h. The blood pressure of the rats in hypertension groups was elevated by 30% with phenylephrine, the rats in contral group and simple is chemic groups were treated with saline infusion. The brain tissues were obtained after killing of all the rats at the t hird、fourth and sixth hour after MCAO, the content of malondialdehyde and the a ctivity of superoxide dismutase(SOD) of brain tissue were examined.Res ults The content of malondialdehyde in simple ischemic group was increa sed obviously comparing with that in control group(P<0.05),And this role increased along with time elapsed; The content of malondialdehyde was decreased obviously by inducing hypertension,the difference between H 3 and I 3 was significant(P<0.05). The activity of SOD in simple i schemic group was decreased comparing with that in control group(P <0.05),and this role becomes bigger and bigger with time elapsed. The activi ty of SOD was increased obviously by inducing hypertension(P<0 .05).The resumed activity of SOD in H 3 and H 4 subgroup was obvious( P<0.05). Conclusion Decreasing the cont ent of malondialdehyde and resuming the activity of SOD may be an important mech anism for treatment of brain ischemia with induced hypertension.

关 键 词：大鼠 脑缺血 升高 对照组 正常 高血压 脑组织 单纯 机制 延长 

分 类 号：R743.3[医药卫生—神经病学与精神病学]