| Long acting calcium antagonist amlodipine prevents left ventricular remodeling after myocardial infarction in rats. | |
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MedLine Citation:
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PMID: 9659445 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: The purpose of this study was to examine the effect of amlodipine, a long-acting calcium antagonist, on the left ventricular remodeling, including systolic and diastolic dysfunction, the change of cardiac gene expression in the myocardial infarcted rats (MI). METHODS: On the first day after myocardial infarction, the animals were randomly assigned to amlodipine treatment (n = 8) or untreated groups (MI; n = 9). We then performed Doppler-echocardiographic examinations and measured the hemodynamics at four weeks after myocardial infarction. Following these measurements, their cardiac mRNA was analyzed. RESULTS: Left ventricular end-diastolic pressure (LVEDP) and central venous pressure (CVP) increased to 22 +/- 1 mmHg and 5 +/- 1 mmHg. Amlodipine reduced LVEDP and CVP to 15 +/- 1 mmHg (P < 0.01) and 3 +/- 0 mmHg (P < 0.01). The weight of right ventricle in MI was significantly larger than in the control rats (Control; 0.48 +/- 0.01 g/kg, MI; 0.79 +/- 0.04 g/kg, P < 0.01). Left ventricular end-diastolic dimension (LVDd) in MI increased to 10.3 +/- 0.3 mm (P < 0.01) (Control; 6.2 +/- 0.3 mm). Amlodipine prevented an increase of the weight of right ventricle (0.62 +/- 0.03 g/kg, P < 0.01) and LVDd (7.9 +/- 0.2 mm, P < 0.01 to MI). The rats in MI showed systolic dysfunction shown by the decreased fractional shortening (Control; 31 +/- 2% versus MI; 15 +/- 1%, P < 0.01), and diastolic dysfunction shown by E wave deceleration rate (Control; 18.1 +/- 2.0 m/s2, MI; 32.6 +/- 2.1 m/s2, P < 0.01). Amlodipine significantly prevented systolic and diastolic dysfunction. The increases in beta-MHC, alpha-skeletal actin, and ANP mRNAs in the non-infarcted left ventricle and right ventricle at four weeks after the myocardial infarction were all significantly suppressed by the treatment with amlodipine. On the other hand, depressed alpha-MHC was restored to normal levels by amlodipine in both regions. CONCLUSIONS: Amlodipine prevents the left ventricular remodeling process accompanied by systolic and diastolic dysfunction, and inhibits abnormal cardiac gene expression after myocardial infarction. |
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Authors:
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T Shimada; M Yoshiyama; K Takeuchi; T Omura; Y Takemoto; S Kim; H Iwao; J Yoshikawa |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Cardiovascular research Volume: 37 ISSN: 0008-6363 ISO Abbreviation: Cardiovasc. Res. Publication Date: 1998 Mar |
Date Detail:
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Created Date: 1998-07-30 Completed Date: 1998-07-30 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0077427 Medline TA: Cardiovasc Res Country: NETHERLANDS |
Other Details:
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Languages: eng Pagination: 618-26 Citation Subset: IM |
Affiliation:
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First Department of Internal Medicine, Osaka City University Medical School, Japan. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Actins
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genetics Amlodipine / therapeutic use* Animals Atrial Natriuretic Factor / genetics Blotting, Northern Calcium Channel Blockers / therapeutic use* Collagen / genetics Echocardiography Gene Expression / drug effects Hemodynamics / drug effects Hypertrophy, Left Ventricular / etiology, prevention & control* Male Myocardial Infarction / complications*, metabolism Myocardium / metabolism* Myosin Heavy Chains / genetics RNA, Messenger / analysis Rats Rats, Wistar Ventricular Dysfunction, Left / etiology, prevention & control* |
| Chemical | |
Reg. No./Substance:
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0/Actins; 0/Calcium Channel Blockers; 0/Myosin Heavy Chains; 0/RNA, Messenger; 85637-73-6/Atrial Natriuretic Factor; 88150-42-9/Amlodipine; 9007-34-5/Collagen |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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