|
|
|
| Systolic pressure and heart heavy index changes in whole process of over-loaded heart hypertrophy |
| LIANG Yue1 ZHANG Guangtao2 TANG Xiaomeng1 WANG Yingchun1 LIU Yuqin1 SHI Jun3 |
1.Department of Pharmacy, Shenzhen Hospital of Peking University, Guangdong Province, Shenzhen 518030, China;
2.Department of Hepatobiliary Surgery, Shenzhen Hospital of Peking University, Guangdong Province, Shenzhen 518030， China;
3.Department of Physiology, Basic Medical College, Inner Mongolia Medical University, Inner Mongolia Autonomous Region, Hohhot 010059, China |
|
|
|
Abstract Objective To discuss the change of systolic pressure and heart weight index (HWI) in the process of cardiovascular pressure overload to myocardial hypertrophy. Methods 80 healthy male Wistar rats were randomly divided into two groups, sham operation group and abdominal aorta group. Each group was randomly separated to 4 time points (3 d, 1 week, 2 weeks, 4 weeks after surgery). Hypertrophy rats model was made by transverse aortic constriction (TAC), systolic blood pressure was measured by noninvasive tail arterial blood pressure measurement and analysis system. The weight of the left ventricular and body was measured by an electronic balance, and the HWI was then calculated. Results Compared with sham operation group, 3 d after TAC surgery, systolic pressure of abdominal aorta group rose, the difference was statistically significant (P < 0.05); 1 week after TAC surgery, systolic pressure of abdominal aorta group rose, HWI increased, the differences were statistically significant (P < 0.05); 2, 4 weeks after TAC surgery, systolic pressure of abdominal aorta group rose, HWI increased, the differences were statistically significant (P < 0.05). Conclusion Rat myocardial hypertrophy model is formed gradually after 1 week and the model is stable in the fourth week. By abdominal TAC, the pressure overload was successfully produced and the myocardial hypertrophy can be induced successfully.
|
|
|
|
|
|
[1] Wright JW，Mizutani S，Harding JW. Pathways involved in the transition from hypertension to hypertrophy to heart failure. Treatment strategies [J]. Heart Fail Rev，2008，13（3）：367-375.
[2] Kehat I，Molkentin JD. Molecular pathways underlying cardiac remodeling during pathophysiological stimulation [J]. Circulation，2010，122（25）：2727-2735.
[3] 赵明月，秦育培，陆立慧，等.压力超负荷所致心肌肥厚中程序性坏死的初步研究[J].生物医学工程学杂志，2015， 32（3）：618-623.
[4] Martinho-Dias D，Leite-Moreira A，Castro-Chaves P. Calreticulin in the heart：from embryological development to cardiac pathology [J]. Curr Mol Med，2016，16（1）：12-22.
[5] Huai Y，Wang H，Zhao L，et al. Lacidipineinbits endoplasmic reticulum stress and myocardial remode-ling induced by pressure overload in rat heart [J]. Eur J Pharmacol，2013， 718（1/3）：441-447.
[6] Cao BQ，Yu Q，Zhao W，et al. Kallikrein-related peptidase 8 is expressed in myocardium and induces cardiac hypertrophy [J]. Sci Rep，2016，6：1-16.
[7] Marketou ME，Parthenakis F，Vardas PE. Pathological left ventricular hypertrophy and stem cells：current evidence and new perspectives [J]. Stem Cells Int，2016，2016：5720758.
[8] Wang N，Cao YS，Zhu Y. Netrin-1 prevents the development of cardiac hypertrophy and heart failure [J]. Mol Med Rep，2016，13（3）：2175-2181.
[9] Cardin S，Guasch E，Luo X，et al. Role for MicroRNA-21 in atrial profibrillatory fibrotic remodeling associated with experimental postinfarction heart failure [J]. Circ Arrhythm Electrophysiol，2012，5（5）：1027-1035.
[10] Aurora AB，Mahmoud AI，Luo X，et al. MicroRNA-214 protects the mouse heart from ischemic injury by controlling Ca2+ overload and cell death [J].J Clin Invest，2012，122（4）：1222-1232.
[11] Anderson PG，Allard MF，Thomas GD，et al.Increased ischemic injury but decreased hypoxic injury in hypertrophied rat heart [J]. Cir Res，1990，67（4）：943-946.
[12] Huang MH，Lui CY，Abusaid GH，et al. Cardiac calcitonin gene-related peptide and left ventricular hypertrophy in the cardiac allograft [J]. J Heart Lung Transplantation，2010，29（4）：487-488.
[13] 程杰坤，李乐.心肌肥厚动物模型建立方法研究进展[J].中国药房，2015，18（25）：3584-3587.
[14] 吴思媛，陆立慧，赵明月，等.钙网蛋白在压力超负荷心肌肥厚中的作用研究[J].生物医学工程学杂志，2016， 33（3）：512-519.
[15] 严思敏，吴双，孙丽，等.大鼠压力负荷增加心肌肥厚模型中核仁素的表达[J].中南大学学报：医学版，2014，39（2）：124-128.
[16] 丁同斌，简立国，张丽华，等.瑞舒伐他汀对心肌肥厚大鼠心肌组织Beclin-1蛋白表达的影响[J].郑州大学学报：医学版，2016，51（2）：251-254.
[17] 王婷，柴春艳，王甜，等.HIF-1α在压力过负荷大鼠心肌组织中的表达[J].心脏杂志，2015，27（6）：662-665.
[18] 郭志坤，武俊芳，单卫华，等.异丙肾上腺素诱导的大鼠肥厚心肌组织中Ⅰ、Ⅲ型胶原蛋白的表达[J].解剖学报，2012，43（1）：92-97.
[19] 黄颖，伍伟锋.自发性高血压大鼠左心室肥厚心肌微小RNA-1及微小RNA-133的差异表达[J].中华高血压杂志，2014，22（12）：1157-1161.
[20] 陈柏荣，刘茂，罗礼云，等.Apelin-13对自发性高血压大鼠心肌肥厚的影响[J].临床和实验医学杂志，2016，15（9）：825-829. |
|
|
|
