| Chronic heart rate reduction facilitates cardiomyocyte survival after myocardial infarction. | |
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MedLine Citation:
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PMID: 20225200 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Chronic heart rate reduction (HRR) therapy following myocardial infarction, using either the pure HRR agent ivabradine or the beta-blocker atenolol, has been shown to preserve maximal coronary perfusion, via reduction of perivascular collagen and a decrease in renin-angiotensin system activation. In addition ivabradine, but not atenolol, treatment attenuated the decline in ejection fraction and decreased left ventricular wall stress. In this study, we tested the hypothesis that cell survival within the infarct region was enhanced by these two pharmacological agents. Four weeks after ligating the left anterior descending coronary artery, the percentage of the LV that contained the infarct was similar in the untreated (MI) rats and those chronically treated with ivabradine (MI + IVA) or atenolol (MI + ATEN). However, the mean thickness (mm) of the ventricular wall containing the scar was significantly greater in the MI + IVA, 1.54 (P < or = 0.01) and the MI + ATEN 1.32, compared to 1.1 in the MI group, due to a 2-fold greater area of surviving cardiomyocytes (P < or = 0.01) in the treated rats compared to the untreated group. Regions of cell survival were usually in the subepicardium, with cardiomyocytes surrounding veins or venules. However, some hearts displayed surviving cells along the endocardium. These data suggest that HRR by either ivabradine or atenolol facilitates a more favorable O2 microenvironment via improved venous flow and decreased O2 demand. We conclude that chronic HRR by these agents may serve to limit infarct expansion and wall thinning and may serve to reduce the potential for ventricular rupture. |
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Authors:
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Rong-Lin Zhang; Lance P Christensen; Robert J Tomanek |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Anatomical record (Hoboken, N.J. : 2007) Volume: 293 ISSN: 1932-8494 ISO Abbreviation: Anat Rec (Hoboken) Publication Date: 2010 May |
Date Detail:
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Created Date: 2010-04-30 Completed Date: 2010-08-10 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 101292775 Medline TA: Anat Rec (Hoboken) Country: United States |
Other Details:
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Languages: eng Pagination: 839-48 Citation Subset: IM |
Affiliation:
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Department of Anatomy and Cell Biology, University of Iowa, Iowa City, Iowa, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Anti-Arrhythmia Agents / pharmacology, therapeutic use Atenolol / pharmacology*, therapeutic use Benzazepines / pharmacology*, therapeutic use Bradycardia / chemically induced Cell Survival / drug effects, physiology Cicatrix / drug therapy, physiopathology Coronary Circulation / drug effects, physiology Diastole / drug effects, physiology Disease Models, Animal Heart Rate / drug effects*, physiology Male Myocardial Infarction / drug therapy*, pathology, physiopathology Myocardium / cytology, metabolism Myocytes, Cardiac / cytology, drug effects*, physiology Rats Rats, Sprague-Dawley Recovery of Function / drug effects*, physiology Regeneration / drug effects, physiology Treatment Outcome |
| Chemical | |
Reg. No./Substance:
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0/Anti-Arrhythmia Agents; 0/Benzazepines; 155974-00-8/ivabradine; 29122-68-7/Atenolol |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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