|本期目录/Table of Contents|

[1]张 凯,王卫定,赵志强,等.慢性间歇缺氧心房重构模型的建立[J].天津医科大学学报,2017,23(06):498-501.
 ZHANG Kai,WANG Wei-ding,ZHAO Zhi-qiang,et al.Establishment of atrial remodeling model with chronic intermittent hypoxia[J].Journal of Tianjin Medical University,2017,23(06):498-501.
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慢性间歇缺氧心房重构模型的建立(PDF)
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《天津医科大学学报》[ISSN:1006-8147/CN:12-1259/R]

卷:
23
期数:
2017年06期
页码:
498-501
栏目:
基础医学
出版日期:
2017-11-20

文章信息/Info

Title:
Establishment of atrial remodeling model with chronic intermittent hypoxia
文章编号:
1006-8147(2017)06-0498-04
作者:
张 凯王卫定赵志强张跃袁 梦李广平
(天津医科大学第二医院心脏科,天津市心血管病离子与分子机能重点实验室,天津心脏病学研究所,天津 300211)

Author(s):
ZHANG Kai WANG Wei-ding ZHAO Zhi-qiang ZHANG Yue YUAN Meng LI Guang-ping
(Department of Cardiology, The Second Hospital , Tianjin Medical University, Tianjin Key Laboratory of Ionic-Molecular Function of Cardiovascular Disease, Tianjin Institute of Cardiology, Tianjin 300211, China)

关键词:
房颤动慢性间歇缺氧模型
Keywords:
atrial fibrillation chronic intermittent hypoxia model
分类号:
R541.7+5
DOI:
-
文献标志码:
A
摘要:
目的:通过慢性间歇缺氧的方法建立大鼠心房颤动(AF)纤维化模型。方法:16只SD雄性大鼠随机分为慢性间歇缺氧组(模型组)和空白对照组,每组8只,慢性间歇缺氧组大鼠置于低压氧舱中,循环充入氮气与氧气,每次循环时间为300 s,其中充入氮气时间为210 s,充入氧气时间为90 s,使舱内氧浓度波动于8%~21%之间。空白对照组普食喂养,未作干预。第31天称重后行超声心动图检查评价心功能并处死大鼠,留取组织进行相应实验,Masson染色并分析心房纤维化程度。结果:模型组大鼠心房纤维化程度与对照组相比明显增加(P<0.05),模型组大鼠肺动脉压力与对照组相比明显升高。结论:慢性间歇缺氧可导致大鼠心房纤维化,其可以被用来作为研究 AF与心房结构重构的重要研究平台。
Abstract:
Objective: To establish fibrosis model of atrial fibrillation(AF) through chronic intermittent hypoxia in rat. Methods: Sixteen SD male rats were randomly divided into chronic intermittent hypoxia group (model group) and control group (n = 8). Model group rats were placed in a chamber, which was periodically filled with nitrogen and oxygen. The time for filling with nitrogen was 210 s, and the time for filling oxygen was 90 s, Concentration of oxygen in chamber was between 8% and 21%. Control group was not intervened. The rats were sacrificed after the examination of echocardiography in the thirty-first day. The tissue of atrial was taken for Masson stain to analyze the degree of atrial fibrosis. Results: The degree of atrial fibrosis in model group was significantly higher than that in control group (P < 0.05). The pressure of pulmonary artery in model group was significantly higher than that in control group. ConclusionChronic intermittent hypoxia can lead to atrial fibrosis in rats, which can be used as an important research platform for AF and atrial remodeling.

参考文献/References:

[1] Wann L S, Curtis A B, January C T, et al. 2011 ACCF/AHA/HRS focused update on the management of patients with atrial fibrillation (Update on Dabigatran)[J]. J Am Coll Cardiol, 2011, 57(11): 1330

[2] Schotten U, Verheule S, Kirchhof P, et al. Pathophysiological mechanisms of atrial fibrillation: A translational appraisal[J]. Physiol Rev, 2011, 91(1): 265

[3] Everett T H 4th, Olgin J E. Atrial fibrosis and the mechanisms of atrial fibrillation[J]. Heart Rhythm, 2007, 4(3 Suppl): 24

[4] Nishida K, Michael G, Dobrev D, et al. Animal models for atrial fibrillation: clinical insights and scientific opportunities[J]. Europace, 2010, 12(2): 160

[5] Riley G, Syeda F, Kirchhof P, et al. An introduction to murine models of atrial fibrillation[J]. Front Physiol, 2012, 8(3): 296

[6] Ramos P, Rubies C, Torres M, et al. Atrial fibrosis in a chronic murine model of obstructive sleep apnea: mechanisms and prevention by mesenchymal stem cells[J]. Respir Res, 2014, 15(1): 54

[7] Qu Y C, Du Y M, Wu S L, et al. Activated nuclear factor-kappaB and increased tumor necrosis factor-alpha in atrial tissue of atrial fibrillation [J]. Scand Cardiovasc J, 2009, 43(5): 292

[8] Katoh Y, Nakazato Y J. Can we predict electroanatomical remodeling of left atrium in patients with non-valvular atrial fibrillation by transforming growth factor-β and tissue inhibitor of metalloproteinase-1[J]. Circ J, 2011, 75(3): 536

[9] Diao S L, Xu H P, Zhang B, et al. Associations of MMP-2, BAX, and Bcl-2 mRNA and protein expressions with development of atrial fibrillation[J]. Med Sci Monit, 2016, 22: 1497

[10] Jalife J, Kaur K. Atrial remodeling, fibrosis, and atrial fibrillation. Trends in cardiovascular medicine[J]. Trends Cardiovasc Med, 2015, 25(6): 475

[11] Wang J, Wang Y, Han J, et al. Integrated analysis of microRNA and mRNA expression profiles in the left atrium of patients with nonvalvular paroxysmal[J]. Heart Rhythm, 2015, 12(5): 1018

[12] Santulli G, Iaccarino G, De Luca N, et al. Atrial fibrillation and microRNAs[J]. Front Physiol, 2014, 5: 15

[13] Barana A, Matamoros M, Dolz-Gaiton P, et al. Chronic atrial fibrillation increases microRNA-21 in human atrial myocytes decreasing L-type calcium current[J]. Circ Arrhythm Electrophysiol, 2014, 7(5): 861

[14]Satoh A, Niwano S, Niwano H, et al. Aliskiren suppresses atrial electrical and structural remodeling in a canine model of atrial fibrillation[J]. Heart Vessels, 2017, 32(1): 90

[15]Fu H, Liu C, Li J, et al. Impaired atrial electromechanical function and atrial fibrillation promotion in alloxan-induced diabetic rabbits[J]. Cardiol J, 2013, 20(1): 59

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备注/Memo

备注/Memo:
基金项目 国家自然科学基金面上项目基金资助(81570304)

作者简介 张凯(1991-),男,硕士在读,研究方向:心律失常;通信作者:李广平,E-mail:tjcardiol@126.com。



更新日期/Last Update: 2017-11-14