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Effects of Benazepril and Irbesartan on Myocardial Remodeling and its Mechanisms in Chronic Heart Failure Rats

Author: RenYaLi
Tutor: XuJiLiang
School: Nantong University
Course: Maritime medicine
Keywords: Ventricular remodeling Angiotensin Ⅱ Angiotensin Ⅱ receptor type 1 Angiotensin II receptor 2 ACE2 p-38MAPK Benazepril Irbesartan Rats with heart failure
CLC: R541.6
Type: Master's thesis
Year: 2008
Downloads: 93
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Abstract


Objective benzene enalapril, irbesartan alone and the efficacy of the combination on ventricular remodeling in heart failure (Chronic Heart Failure, CHF) rats to observe the myocardial tissue of AT1R of angiotensin Ⅱ type 2 receptor, ACE2, p-38MAPK and p-of p38MAPK changes in protein expression, to explore the depth mechanism of the the benzene that rats with heart failure in Plymouth and irbesartan anti-ventricular remodeling. Methods abdominal aortic coarctation caused by pressure overload cardiac hypertrophy induced rat model of heart failure. Into sham operation group (Con group), model group (Mod group), benazepril treatment group (Ben group, 10 mg · kg-1 · d-1), irbesartan treatment group (Irb group 50mg · kg- 1 · d-1) and the combined treatment group (Com Group Ben 5mg · kg-1 · d-1 Irb 25mg · kg-1 · d-1) ig 8 weeks, systolic blood pressure was measured every two weeks. Echocardiography in detecting cardiac configuration and ejection function, hemodynamic parameters measured carotid artery catheter; detection of cardiac index, myocardial cell size of cardiac hypertrophy indicators; determination of ventricular tissue hydroxyproline content, restrictive pepsin degradation method to evaluate myocardial collagen cross-linking degree of a comprehensive evaluation of myocardial tissue fibrosis; radioimmunoassay determination of myocardial and plasma Ang Ⅱ content; immunohistochemistry method for the determination of changes in the myocardial tissue of type I collagen, type III collagen, AT1R and AT2R protein levels ; the protein blotting myocardial tissue of AT1R of angiotensin Ⅱ type 2 receptor, ACE2, p-38MAPK and p-p38MAPK protein expression. Results Mod lowered the blood pressure is lower than the Con group; blood pressure in all treatment groups compared with Mod group decreased, but no significant difference. Compared with Con Mod group, left ventricular systolic diameter (LVSD), left ventricular end-diastolic diameter (LVDD), left ventricular end-diastolic pressure (LVEDP) was significantly higher, while the ejection fraction (EF) was significantly reduced; with the the Mod group of each treatment group compared to LVSD, LVDD, LVEDP significantly reduced EF significantly higher, combination therapy is superior to single, and improve heart function. Compared with Con Mod group cardiac index, the size of the myocardial cells, myocardial hydroxyproline content, myocardial interstitial and perivascular collagen area and collagen cross-linking degree was significantly higher; each treatment group it decreased joint application have a synergistic effect, thereby improving cardiac hypertrophy and myocardial fibrosis. Mod plasma and myocardial tissue Ang Ⅱ level was significantly higher than Con group; decreased the Ben group with Com group, Irb group was significantly higher. 5 compared with the Con group, MOD group of type I collagen, type III collagen, AT1R, AT2R in, ACE2, p-p38MAPK in significantly increased, p-38MAPK no significant change; treatment group of type I collagen, type III collagen, AT1R p-p38MAPK was significantly reduced, AT2R, ACE2 was significantly higher, p-38MAPK no significant change, combined with a synergistic effect. Conclusion that benzene Plymouth and irbesartan alone may reduce ventricular remodeling in rats with heart failure and improve cardiac function, combined with a synergistic effect, may be associated with the regulation in rats with heart failure circulation and myocardial Ang Ⅱ level, affecting myocardial I type collagen, type III collagen, AT1R, AT2R in ACE2 in, the p-38MAPK and p-p38MAPK protein expression.

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CLC: > Medicine, health > Internal Medicine > Heart, blood vessels ( circulatory ) disease > Heart disease > Blood circulation failure
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