中国组织工程研究 ›› 2016, Vol. 20 ›› Issue (40): 6007-6013.doi: 10.3969/j.issn.2095-4344.2016.40.012

• 心血管损伤动物模型 Animal models of cardiovascular damage • 上一篇    下一篇

运动性心肌缺血损伤模型大鼠的制备

彭峰林1,黄丽丽2,郭艳菊1   

  1. 1广西师范大学体育学院,广西壮族自治区桂林市 541004;2开平市忠源纪念中学,广东省开平市 529300)
  • 修回日期:2016-08-07 出版日期:2016-09-30 发布日期:2016-09-30
  • 作者简介:彭峰林,男,1969年生,湖南省双峰县人,汉族,2007年华南师范大学毕业,博士,教授,主要从事心血管运动适应的生物学机制研究。
  • 基金资助:

    广西科技基础条件平台建设项目(12-97-24):运动性心肌缺血损伤大鼠模型的构建与评估;国家自然科学基金(31060146):K(ATP)的运动适应性变化在提高心肌缺血耐受性中的作用及其信号转导途径;国家自然科学基金(31560291):运动预适应提高心肌缺血耐受性的自噬调控机制研究

Rat model of exercise-induced myocardial ischemia injury

Peng Feng-lin1, Huang Li-li2, Guo Yan-ju1   

  1. 1Sport School of Guangxi Normal University, Guilin 541004, Guangxi Zhuang Autonomous Region, China; 2Kaiping City Zhong Source Memorial Middle School, Kaiping 529300, Guangdong Province, China
  • Revised:2016-08-07 Online:2016-09-30 Published:2016-09-30
  • About author:Peng Feng-lin, M.D., Professor, Sport School of Guangxi Normal University, Guilin 541004, Guangxi Zhuang Autonomous Region, China
  • Supported by:

    the National Natural Science Foundation of China, No. 31060146, 31560291; the Construction Project of Science & Technology Infrastructure of Guangxi Zhuang Autonomous Region, No. 12-97-24

摘要:

文章快速阅读:


文题释义:
运动性心肌缺血:随着运动负荷的增加,当心肌的氧供与氧需失去平衡或内环境失调致心肌获取不到充足的氧量时,心肌表现为相对缺血状态,心肌对相对缺血有一定的耐受性,但超过阈值则会导致心肌出现不可逆损伤。
力竭运动:某一运动强度下长时间运动,直到完全无力维持运动,表现为精疲力竭。强度越高,达到力竭的时间越短。
 
摘要
背景:运动性心肌缺血动物模型的建立没有统一的标准,导致研究结果的不可比性,影响了运动医学特别是运动心血管领域研究的推进,所以建立统一的运动性心肌缺血动物模型势在必行。
目的:探索建立跑台运动性心肌缺血损伤大鼠模型的方法。
方法:96只SD雌性大鼠被随机分为安静对照组、异丙肾上腺素药物模型组和10个运动组(中强度力竭运动1,3次组、中强度力竭运动1,2,3周组、高强度力竭运动1,3次组、高强度力竭运动1,2,3周组),取各组心肌组织进行苏木精-伊红染色病理分析,检测血清心肌酶指标和肌钙蛋白I水平,RT-PCR检测bcl-2bax基因表达。
结果与结论:①心肌苏木精-伊红染色检测结果:随着运动时间的延长损伤程度越来越严重,且高强度运动组比中强度运动组损伤程度更严重;②血清心肌酶指标和肌钙蛋白I水平:中强度力竭运动自1周开始,血清谷草转氨酶与乳酸脱氢酶活性出现显著性升高(P < 0.05或P < 0.01),高强度力竭性运动训练3次开始,谷草转氨酶与乳酸脱氢酶活性显著性升高(P < 0.05或P < 0.01)。各组肌钙蛋白I含量的变化趋势与谷草转氨酶、乳酸脱氢酶活性变化基本相同,但中强度力竭运动需2周肌钙蛋白I含量才比安静对照组显著升高;③细胞凋亡调控基因表达:各运动组bcl-2/bax比值均显著性低于安静对照组(P < 0.05或P < 0.01),高强度1次组(P < 0.01)和3次组(P < 0.05)明显高于异丙肾上腺素药物模型组,中强度各组均高于异丙肾上腺素药物模型组(P < 0.05或P < 0.01);④结果表明,中强度跑台力竭运动3周开始、高强度跑台力竭运动2周开始的运动模型都可作为运动性心肌缺血损伤模型,病理分析、心肌血清酶谱、肌钙蛋白I可作为建立运动性心肌缺血损伤模型的评估指标,细胞凋亡调控基因只可作为参考指标。

中国组织工程研究杂志出版内容重点:肾移植肝移植移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植组织工程

ORCID:
0000-0002-8640-035X(彭峰林)

关键词: 实验动物, 心血管及肺损伤与修复动物模型, 运动性心肌缺血损伤, 力竭运动, 跑台运动, 大鼠, 模型, 国家自然科学基金

Abstract:

BACKGROUND: No uniform standard for constructing the animal model of exercise-induced myocardial ischemia injury results in the incomparability among research results and impedes the development of sport medicine especially in the cardiovascular field; thereby, it is imperative to reach an agreement in constructing criteria.

OBJECTIVE: To explore the method of establishing the rat model of myocardial ischemia induced by running.
METHODS: Totally 96 female Sprague-Dawley rats were randomly divided into rest control group, isoprenaline group and 10 exercise groups (1- and 3-time moderate-intensity exercise groups, 1-, 2- and 3-week moderate-intensity exercise groups, 1- and 3-time high-intensity exercise groups, 1-, 2- and 3-week high-intensity exercise groups). After exhaustive exercise, myocardium was collected for morphological observation by hematoxylin-eosin staining, serum levels of myocardial enzymes and cardiac troponin I were detected, and the expressions of Bcl-2 and Bax were detected by real-time PCR.

RESULTS AND CONCLUSION: (1) Hematoxylin-eosin staining showed that the damage degree was more severe with the time of exercise, and the high-intensity exercise groups were more severe than those in the moderate-intensity exercise groups. (2) The activity of serum glutamic-oxaloacetic transaminase and lactic dehydrogenase was significantly increased after 1-week moderate-intensity exhaustive exercise (P < 0.05 or P < 0.01). From the beginning of the 3-time high-intensity exhaustive exercise, the activity of glutamic-oxaloacetic transaminase and lactic dehydrogenase was significantly increased (P < 0.05 or P < 0.01). (3) Cardiac troponin I content change trend was basically the same as glutamic-oxaloacetic transaminase and lactic dehydrogenase changes, but cardiac troponin I content in the moderate-intensity exhaustive exercise groups was significantly higher than that in the rest control group until 2 weeks. The Bcl-2/Bax ratios in all exercise groups were significantly lower than that in the rest control group (P < 0.05 or P < 0.01); those in the 1- and 3-time high-intensity exercise groups were significantly higher than in the isoprenaline group (P < 0.05 or P < 0.01); and those in moderate-intensity groups were higher than in the isoprenaline group (P < 0.05 or P < 0.01). (4) In conclusion, 2-week high-intensity and 3-week moderate-intensity exhaustive exercise can induce myocardial ischemia injury, and pathological analysis, serum levels of myocardial enzymes and cardiac troponin I can be used as the evaluation indexes, while apoptosis regulation genes just as the reference index.

中国组织工程研究杂志出版内容重点:肾移植肝移植移植;心脏移植;组织移植;皮肤移植;皮瓣移植;血管移植;器官移植组织工程

Key words: Myocardial Ischemia, Athletic Injuries, Hyperkinesis, Tissue Engineering

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