| Physical training alters the pathogenesis of pacing-induced heart failure through endothelium-mediated mechanisms in awake dogs. | |
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MedLine Citation:
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PMID: 9355910 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Beneficial effects of exercise training on cardiovascular function in chronic heart failure (CHF) have been suggested previously, but the underlying mechanisms are unknown. We tested whether daily exercise training improves systemic hemodynamics and preserves endothelium-mediated vasodilator function during development of heart failure. METHODS AND RESULTS: Fifteen dogs were surgically instrumented for hemodynamic measurements. One group of dogs underwent 4 weeks of cardiac pacing (210 bpm for 3 weeks and 240 bpm during week 4), and another group underwent pacing plus daily exercise training (4.4+/-0.3 km/h, 2 h/d). Pacing-alone dogs developed CHF characterized by typical hemodynamic abnormalities, blunted endothelium-mediated vasodilator function in coronary and femoral circulations, and decreased gene expression of endothelial constitutive nitric oxide synthase (ECNOS, normalized to GAPDH expression; normal, 1.15+/-0.31 versus CHF, 0.29+/-0.08, P<.05). Exercise training preserved normal hemodynamics at rest, endothelium-mediated vasodilator function, and gene expression of ECNOS (0.72+/-0.16 versus normal, P=NS). Inhibition of NO synthesis (nitro-L-arginine) in exercise-trained dogs abolished the preserved endothelium-mediated vasodilation of epicardial coronary arteries and elevated left ventricular end-diastolic pressure (7.7+/-0.3 to 19+/-3.4 mm Hg, P<.05), suggesting that the preservation of resting hemodynamics was in large part due to preserved endothelial function concealing the underlying CHF state. CONCLUSIONS: Long-term exercise training altered the natural history of heart failure due to rapid cardiac pacing. One of the underlying mechanisms is through the preservation of endothelial vasodilator function. |
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Authors:
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J Wang; G H Yi; M Knecht; B L Cai; S Poposkis; M Packer; D Burkhoff |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Circulation Volume: 96 ISSN: 0009-7322 ISO Abbreviation: Circulation Publication Date: 1997 Oct |
Date Detail:
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Created Date: 1997-12-09 Completed Date: 1997-12-09 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 0147763 Medline TA: Circulation Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 2683-92 Citation Subset: AIM; IM |
Affiliation:
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Department of Medicine and Institute of Comparative Medicine, College of Physicians and Surgeons of Columbia University, New York City, NY 10032, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Body Weight Cardiac Pacing, Artificial Disease Models, Animal Dogs Endothelium, Vascular / enzymology, physiopathology* Female Gene Expression Regulation, Enzymologic Glyceraldehyde-3-Phosphate Dehydrogenases / genetics, metabolism Heart Failure / enzymology, physiopathology*, prevention & control Heart Rate Hemodynamics Male Nitric Oxide Synthase / genetics, metabolism Organ Size Physical Conditioning, Animal* Vasodilation |
| Grant Support | |
ID/Acronym/Agency:
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1-R-29-HL-51885-01/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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EC 1.14.13.39/Nitric Oxide Synthase; EC 1.2.1.-/Glyceraldehyde-3-Phosphate Dehydrogenases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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