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作 者:娄金丽[1] 张允岭[1] 郝然[2] 刘超[1] 郑宏[1] 黄启福[2]
机构地区:[1]北京中医药大学东方医院,北京100078 [2]北京中医药大学基础医学院
出 处:《北京中医药大学学报》2007年第11期740-743,I0001,共5页Journal of Beijing University of Traditional Chinese Medicine
基 金:国家重点基础研究发展计划("973"计划)资助项目(No.2006CB504805);教育部新世纪优秀人才支持计划(No.NCET-05-0139)
摘 要:目的探讨急性脑缺血过程存在毒损脑络进而损及心络的机制,为内毒损伤络脉学说提供实验依据。方法线栓法阻塞大鼠大脑中动脉建立急性脑梗死模型;检测脑梗死模型大鼠血清肌酸激酶同工酶(CK-MB)活性、心电图及心脏病理形态学改变;放免法检测心肌组织内皮素(ET)变化,生化法检测心肌组织一氧化氮(NO)、丙二醛(MDA)、超氧化物歧化酶(SOD)等变化。结果脑梗死大鼠血清CK-MB活性增高(P<0.01),心电图出现ST段下降,或T波低平、倒置等心肌缺血性改变;光镜下可见心肌细胞的早期病变;电镜下可见心肌细胞线粒体肿胀、肌原纤维横纹和线粒体嵴模糊不清、细胞间质水肿等。ET/NO、MDA、SOD等指标发生了异常改变(P<0.01)。结论急性脑缺血伴发有心肌细胞损害;血管活性物质、氧自由基等毒性效应导致了心肌组织损害过程,体现出内毒损伤脑络进而损及心络的机制。Objective To Explore the mechanism of internal toxin damaging brain collaterals and then heart collaterals in the myocardial injury caused by acute cerebral ischemia. Methods Rat model with middle cerebral artery occlusion (MCAO) was established with thread occlusion technique. Serum CK- MB activity, ECG and pathological morphological changes of myocardial tissue structure were detected in acute cerebral ischemia. Endothelin (ET) in myocardial tissue was detected by RIA. Nitric oxide ( NO), malondialdehyde (MDA) and superoxide dismutase (SOD) in myocardial tissue were measured by biochemical methods. Results The CK-MB activity in serum increased ( P 〈 0.01 ). ECG showed descended ST segment, lowed or inversed T wave. Cardiocyte early pathological changes could be observed under the light microscope. Mitochondria swelling, myofibril transverse striation and mitochondria cristae unclearing and mesenchyme edema could be observed under the electric microscope. ET/NO, MDA and SOD also altered significantly ( P 〈 0.01 ). Conclusion Acute cerebral isehemia may cause myocardial injury. The toxin effect of Vasoactive substance and free radical etc. resulted in myocardial injury. All these clarify the mechanism of internal toxin damaging brain collaterals and thenheart collaterals.
分 类 号:R228[医药卫生—中医基础理论]
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