|本期目录/Table of Contents|

[1]徐凯月,孟祥雪,黄 传,等.间歇性低氧干预提高心梗大鼠心功能和运动耐量[J].天津医科大学学报,2019,25(05):459-462.
 XU Kai-yue,MENG Xiang-xue,HUANG Chuan,et al.Intermittent hypoxia intervention improves cardiac function and exercise tolerance of rats with myocardial infarction[J].Journal of Tianjin Medical University,2019,25(05):459-462.
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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
25
期数:
2019年05期
页码:
459-462
栏目:
基础医学
出版日期:
2019-09-20

文章信息/Info

Title:
Intermittent hypoxia intervention improves cardiac function and exercise tolerance of rats with myocardial infarction
文章编号:
1006-8147(2019)05-0459-04
作者:
徐凯月孟祥雪黄 传史 昱万春晓
(天津医科大学总医院康复医学科,天津300052)
Author(s):
XU Kai-yue MENG Xiang-xue HUANG Chuan SHI Yu WAN Chun-xiao
(Department of Physical and Rehabilitation Medicine, General Hospital, Tianjin Medical University, Tianjin 300052, China)
关键词:
间歇性低氧心肌梗死心功能运动耐量AMPK
Keywords:
intermittent hypoxia myocardial infarction cardiac function exercise tolerance AMPK
分类号:
R54
DOI:
-
文献标志码:
A
摘要:
目的:观察4周间歇性低氧(IH)干预对心梗(MI)大鼠心功能及运动耐量的影响。方法:28只雄性SD大鼠随机分为4组:空白组(Sham)、空白低氧组(Sham-IH)、心梗组(MI)和心梗低氧组(MI-IH)。低氧组放入低氧仓(模拟海拔5 000 m,氧浓度13%),每天4 h。对照组置于常氧环境中。干预4周后检测心肌AMPK表达,心梗面积比例,左心室射血分数和运动耐量。结果:同MI组比较,MI-IH组 (1) 心梗面积比例减少(P<0.001);(2) 左心室射血分数增加(P<0.001);(3) 运动耐量增加(P<0.001);(4) AMPK表达增加(P<0.05)。结论:4周间歇性低氧干预能提高心功能和运动耐量,可能与心肌AMPK表达增加有关。
Abstract:
Objective: To explore the effects of four-week intermittent hypoxia (IH) intervention on cardiac function and exercise tolerance in rats with myocardial infarction (MI). Methods: Twenty-eight male SD rats were randomly divided into four groups: Sham group, Sham-IH group, MI group and MI-IH group. The IH groups were placed in the hypoxic chamber (simulates 5 000 maltitude, 13% oxygen concentration), at 4 h/d. The control groups were placed in normal environment. The AMPK expression, infarct size ratio, left ventricular ejection fraction and exercise tolerance were measured after 4-week intervention. Results: Compared with MI group, MI-IH group showed (1) decreased infarct size ratio (P <0.001);(2) increased left ventricular ejection fraction(P <0.001);(3) increased the exercise tolerance (P <0.001);(4) increased the expression of AMPK(P <0.05). Conclusion: 4-week IH intervention can improve cardiac function and exercise tolerance in rats with MI, which may be related to AMPK elevation.

参考文献/References:

[1] Writing Group Members, Mozaffarian D, Benjamin E J, et al. Executive summary: heart disease and stroke statistics-2016 update: a report from the American heart association[J]. Circulation,2016,133(4):447
[2] Wan C X, Lan Y F, Jiang H, et al. Hypoxia training attenuates left ventricular remodeling in rabbit with myocardial infarction[J]. J Geriatr Cardiol, 2014, 11(3):237
[3] Buckley J P, Furze G, Doherty P, et al. BACPR scientific statement: British standards and core components for cardiovascular disease prevention and rehabilitation[J]. Heart, 2013, 99(15):1069
[4] Gu S, Hua H, Guo X Q, et al. PGC-1α participates in the protective effect of chronic intermittent hypobaric hypoxia on cardiomyocytes[J]. Cell Physiol Biochem, 2018, 50(5):1891
[5] Zheng C, Lin J F, Lin Z H, et al. Sodium houttuyfonate alleviates post-infarct remodeling in rats via AMP-Activated protein kinase pathway[J]. Front Pharmacol, 2018, 9:1092
[6] Peng W, Zhang Y, Zhu W Z, et al.AMPK and TNF-alpha at the crossroad of cell survival and death in ischaemic heart[J]. Cardiovasc Res, 2009,84(1):1
[7] Castanares-Zapatero D, Bouleti C, Sommereyns C, et al.Connection between cardiac vascular permeability, myocardial edema, and inflammation during sepsis: role of the alpha(1)AMP-Activated protein kinase isoform[J]. Crit Care Med, 2013,41(12):E411
[8] Hardie D G, Ross F A, Hawley S A. AMPK: a nutrient and energy sensor that maintains energy homeostasis[J]. Nat Rev Mol Cell Biol, 2012,13(4):251
[9] Campbell M D, Duan J, Samuelson A T, et al. Improving mitochondrial function with SS-31 reverses age-related redox stress and improves exercise tolerance in aged mice[J].Free Radic Biol Med,2018, 134:268
[10] Moreira J B, Bechara L R,Bozi L H, et al. High- versus moderate-intensity aerobic exercise training effects on skeletal muscle of infarcted rats[J]. J Appl Physiol (1985),2013,114(8):1029
[11] Roger V L, Go A S, Lloyd-Jones D M, et al. Heart disease and stroke statistics--2012 update: a report from the American Heart Association[J]. Circulation, 2012,125(1):e2
[12] Lien C F, Lee W S, Wang I C, et al. Intermittent hypoxia-generated ROS contributes to intracellular zinc regulation that limits ischemia/reperfusion injury in adult rat cardiomyocyte[J]. J Mol Cell Cardiol,2018,118:122
[13] Van Hout G P,Teuben M P,Heeres M, et al. Invasive surgery reduces infarct size and preserves cardiac function in a porcine model of myocardial infarction[J]. J Cell Mol Med, 2015,19(11):2655
[14] Dagres N, Hindricks G. Risk stratification after myocardial infarction: is left ventricular ejection fraction enough to prevent sudden cardiac death[J]. Eur Heart J, 2013,34(26):1964
[15] Perelshtein Brezinov O, Klempfner R, Zekry S B, et al.Prognostic value of ejection fraction in patients admitted with acute coronary syndrome: a real world study[J]. Medicine (Baltimore), 2017,96(9):e6226
[16] Kato M, Kubo A, Nihei F, et al. Effects of exercise training on exercise capacity,cardiac function, BMI, and quality of Life in patients with atrial fibrillation:a meta-analysis of randomized-controlled trials[J]. Int J Rehabil Res, 2017,40(3):193
[17] Reibis R K, Treszl A, Wegscheider K, et al. Exercise capacity is the most powerful predictor of 2-year mortality in patients with left ventricular systolic dysfunction[J]. Herz, 2010,35(2):104
[18] Papasavvas T, Alhashemi M, Micklewright D. Association between depressive symptoms and exercise capacity in patients with heart disease: a meta-analysis[J]. J Cardiopulm Rehabil Prev, 2017, 37(4):239
[19] Myers J, Prakash M, Froelicher V, et al. Exercise capacity and mortality among men referred for exercise testing[J]. N Engl J Med, 2002, 346(11):793
[20] Ma X W, Fu Y N, Xiao H, et al. Cardiac fibrosis alleviated by exercise training is AMPK-Dependent[J]. PLoS One, 2015,10(6):e0129971
[21] Kim A S, Miller E J, Wright T M, et al. A small molecule AMPK activator protects the heart against ischemia-reperfusion injury[J]. J Mol Cell Cardiol, 2011, 51(1):24

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备注/Memo

备注/Memo:
基金项目 天津市卫生局2016年重点发展项目(16KJ122),天津市自然科学基金重点项目(18JCZDJC98900)
作者简介 徐凯月(1994-),女,硕士在读,研究方向:心脏康复;通信作者:万春晓,E-mail:wcx2226@163.com。
更新日期/Last Update: 2019-10-11