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[1]刘雪梅,陶冶,傅晨,等.从“脑心同病”探讨急性脑缺血引发心肌损伤的动态变化[J].环球中医药,2016,9(09):1047-1051.[doi:10.3969/j.issn.1674-1749.2016.09.004]
　LIU Xue-mei,TAO Ye,FU Chen,et al.Dynamic change from the “Naoxin Tongbing” on myocardial injury induced by acute cerebral ischemia[J].,2016,9(09):1047-1051.[doi:10.3969/j.issn.1674-1749.2016.09.004]
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从“脑心同病”探讨急性脑缺血引发心肌损伤的动态变化()
     
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《环球中医药》[ISSN:1006-6977/CN:61-1281/TN]

卷:
第9卷
期数:
2016年09期
页码:
1047-1051
栏目:
论著
出版日期:
2016-09-06

文章信息/Info

Title:
Dynamic change from the “Naoxin Tongbing” on myocardial injury induced by acute cerebral ischemia
作者:
刘雪梅; 陶冶; 傅晨; 王凤丽; 郑宏; 张允岭
100078 北京中医药大学东方医院实验中心[刘雪梅、陶冶、傅晨、王凤丽、郑宏、张允岭]
Author(s):
LIU Xue-mei;  TAO Ye;  FU Chen; et al.
Dongfang Hospital of Beijing University of Chinese Medicine, Beijing 100078,China
关键词:
急性脑缺血;  心肌损伤;  脑心同病
Keywords:
Acute cerebral ischemia;  Cardiac injury;  Naoxin Tongbing
分类号:
R542.2
DOI:
10.3969/j.issn.1674-1749.2016.09.004
文献标志码:
-
摘要:
目的 观察脑缺血不同时间引发心肌损伤的变化,明确“脑心同病”的生物学基础。方法 电凝法致大脑中动脉闭塞建立急性脑缺血诱发心肌损伤大鼠模型,随机分为正常组、假手术组、缺血6小时模型组、缺血12小时模型组和缺血24小时模型组,每组9只,记录心电图分析心率变异性,ELISA法测定血清肌酸激酶同工酶(creatine kinase MB isoenzyme,CK-MB)活性、心肌肌钙蛋白I(cardiac troponinI,cTnI)含量,HE染色法观察脑、心组织形态学变化,HBFP染色法观察心肌纤维形态学变化。结果 急性脑缺血明显降低中频段、高频段、总频段,中频段与高频段比值随缺血时间延长呈逐渐上升趋势; 随脑缺血时间延长,CK-MB、CTnI呈现先升高后降低趋势,在缺血6小时达高峰; 脑缺血6小时出现神经细胞肿胀、结构不清,部分胞核缩小并深染等缺血改变,随脑缺血时间延长逐渐加重,至脑缺血24小时神经细胞数目明显减少,结构形态破坏严重。心肌细胞胞浆着色不均,心肌嗜酸性变; 脑缺血6小时心肌纤维广泛、弥漫亲复红染色,心肌发生早期病变,随脑缺血时间延长心肌病变逐渐缩小、程度减轻。结论 急性脑缺血能够引发心肌损伤,心肌发生早期病变,心肌酶谱发生异常,可增加心肌酶活性、cTnI含量,在脑缺血6小时达到高峰,证实了脑心同病的生物学基础。
Abstract:
Objective To observe the dynamic change of myocardial injury induced by cerebral ischemia, and determine the biological basis of “Naoxin Tongbing”. Methods Rat model of middle cerebral artery occlusion was established by electro-coagulation technique. Rats were randomly divided into five groups: normal group, sham group, ischemia 6 h, 12 h, 24 h model groups. Heart rate variability was recorded by ECG; Creatine kinase MB isoenzyme(CK-MB)activity, cardiac troponinI(cTnI)content was detected by ELISA; Morphological changes of cerebral tissue was observed by HE staining and HBFP staining. Results Acute cerebral ischemia could decrease MF, HF and TF, MF/HF has an increased tendency. Serum CK-MB activity and cTnI content was increased at first and then decreased,which peaked at 6 h of ischemia. HE staining in the cerebral tissues showed the phenomena of disorganization,neurons edema, quantity decreased and nuclear condensation. The cardiac tissue of HE staining showed chromatosis light, mild coagulation necrosis; 6 hours after cerebral ischemia, myocardial fibers were extensive and diffuse, and the early pathological changes were gradually reduced, and the extent of myocardial lesions decreased with the time of ischemia. Conclusion Acute cerebral ischemia could cause myocardial injury and lead to early myocardial change, increased serum CK-MB activity and cTnI content, which peaked at 6h of cerebral ischemia. It was confirmed the biological basis of “Naoxin Tongbing”.

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备注/Memo

备注/Memo:
基金项目: 国家重点基础研究发展计划(973计划)(2012CB518406); 国家国际科技合作专项(2015DFA31130); 国家自然科学基金(81173233)
作者简介: 刘雪梅(1979- ),女,博士,副研究员。研究方向:中西医结合脑病基础研究。E-mail:liuxuemei04@126.com
通讯作者: 张允岭(1963- ),博士,教授,博士生导师。研究方向:中医脑病临床与机制研究。E-mail:yunlingzhang2004@163.com
更新日期/Last Update: 2016-09-06