| Exercise improves flow-mediated vasodilatation of skeletal muscle arteries in rats with chronic heart failure. Role of nitric oxide, prostanoids, and oxidant stress. | |
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MedLine Citation:
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PMID: 10359741 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Flow-mediated dilatation (FMD) of the peripheral arteries may be impaired in chronic heart failure (CHF), and this could contribute to the increased peripheral resistance and exercise intolerance that occur with this disease. Physical exercise improves the FMD of large conduit arteries in CHF, but whether a similar impairment also occurs in smaller arteries is unknown. The mechanisms of the changes in FMD after CHF or exercise are also unknown. METHODS AND RESULTS: FMD was assessed in isolated, perfused, and preconstricted gracilis muscle arteries from sham-operated rats or CHF rats (coronary artery ligation) who were either sedentary or exercised (30-minute swimming period twice a day for 10 weeks, starting 7 days after ligation). In animals with hemodynamic and echographic signs of CHF, FMD was abolished and converted into vasoconstriction (percent change in diameter after 370 microL/min flow: sham, 42+/-5%; CHF, -4+/-3%; P<0.05). Exercise partially restored FMD (18+/-3%; P<0.05 versus CHF). In sham rats, FMD was abolished by the nitric oxide-synthase inhibitor Nomega-nitro-L-arginine (L-NA) but unaffected by the cyclooxygenase inhibitor diclofenac or the free radical scavenger N-(2-mercaptopropionyl)-glycine (MPG). In arteries from sedentary CHF rats, FMD was not modified by L-NA, but it was partially restored by diclofenac or MPG. In exercised CHF rats, FMD was abolished by L-NA and only moderately improved by diclofenac or MPG. Likewise, endothelial nitric oxide synthase mRNA expression (determined by reverse transcription polymerase chain reaction at the level of the gracilis muscle) was reduced by CHF, and this was prevented by exercise. CONCLUSIONS: CHF abolishes the FMD of small arteries by impairing the nitric oxide pathway, increasing oxidant stress, and releasing a prostanoid-contracting factor. Exercise partially restores FMD by increasing expression of endothelial nitric oxide synthase and preventing the production of vasoconstrictor prostanoids and free radicals. Such restoration of FMD might contribute to the increase in exercise capacity after physical exercise in CHF. |
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Authors:
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R Varin; P Mulder; V Richard; F Tamion; C Devaux; J P Henry; F Lallemand; G Lerebours; C Thuillez |
Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Circulation Volume: 99 ISSN: 1524-4539 ISO Abbreviation: Circulation Publication Date: 1999 Jun |
Date Detail:
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Created Date: 1999-06-24 Completed Date: 1999-06-24 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: 2951-7 Citation Subset: AIM; IM; S |
Affiliation:
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Department of Pharmacology, VACOMED, Rouen University Medical School, Rouen, France. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arteries / physiopathology Cardiac Output, Low / pathology, physiopathology* Chronic Disease Echocardiography Hemodynamics / physiology Male Muscle, Skeletal / blood supply* Myocardium / pathology Nitric Oxide / physiology Nitric Oxide Synthase / metabolism Nitric Oxide Synthase Type III Oxidative Stress / physiology Physical Conditioning, Animal / physiology* Prostaglandins / physiology Rats Rats, Wistar Regional Blood Flow / physiology Vasodilation / physiology* |
| Chemical | |
Reg. No./Substance:
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0/Prostaglandins; 10102-43-9/Nitric Oxide; EC 1.14.13.39/Nitric Oxide Synthase; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, rat |
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