| Reactive oxygen species are critical mediators of coronary collateral development in a canine model. | |
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MedLine Citation:
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PMID: 12816750 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Recent evidence suggests that reactive oxygen species (ROS) promote proliferation and migration of vascular smooth muscle (VSMC) and endothelial cells (EC). We tested the hypothesis that ROS serve as crucial messengers during coronary collateral development. Dogs were subjected to brief (2 min), repetitive coronary artery occlusions (1/h, 8/day, 21 day duration) in the absence (occlusion, n = 8) or presence of N-acetylcysteine (NAC) (occlusion + NAC, n = 8). A sham group (n = 8) was instrumented identically but received no occlusions. In separate experiments, ROS generation after a single 2-min coronary artery occlusion was assessed with dihydroethidium fluorescence. Coronary collateral blood flow (expressed as a percentage of normal zone flow) was significantly increased (71 +/- 7%) in occlusion dogs after 21 days but remained unchanged (13 +/- 3%) in sham dogs. Treatment with NAC attenuated increases in collateral blood flow (28 +/- 8%). Brief coronary artery occlusion and reperfusion caused ROS production (256 +/- 33% of baseline values), which was abolished with NAC (104 +/- 12%). Myocardial interstitial fluid produced tube formation and proliferation of VSMC and EC in occlusion but not in NAC-treated or sham dogs. The results indicate that ROS are critical for the development of the coronary collateral circulation. |
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Authors:
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Weidong Gu; Dorothee Weihrauch; Katsuya Tanaka; John P Tessmer; Paul S Pagel; Judy R Kersten; William M Chilian; David C Warltier |
Publication Detail:
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Type: Journal Article; Research Support, U.S. Gov't, P.H.S. Date: 2003-06-19 |
Journal Detail:
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Title: American journal of physiology. Heart and circulatory physiology Volume: 285 ISSN: 0363-6135 ISO Abbreviation: Am. J. Physiol. Heart Circ. Physiol. Publication Date: 2003 Oct |
Date Detail:
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Created Date: 2003-09-12 Completed Date: 2003-10-10 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 100901228 Medline TA: Am J Physiol Heart Circ Physiol Country: United States |
Other Details:
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Languages: eng Pagination: H1582-9 Citation Subset: IM |
Affiliation:
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Department of Anesthesiology, Medical College of Wisconsin, 8701 Water-town Plank Road, Milwaukee, WI 53226, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Cell Division Collateral Circulation* Coronary Circulation* Coronary Disease / metabolism, pathology, physiopathology* Coronary Vessels / metabolism, pathology Dogs Endothelial Growth Factors / metabolism Endothelium, Vascular / pathology Extracellular Space / metabolism Intercellular Signaling Peptides and Proteins / metabolism Lymphokines / metabolism Muscle, Smooth, Vascular / pathology Myocardium / metabolism Neovascularization, Pathologic Reactive Oxygen Species / metabolism* Vascular Endothelial Growth Factor A Vascular Endothelial Growth Factors |
| Grant Support | |
ID/Acronym/Agency:
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HL-54820/HL/NHLBI NIH HHS; HL-63705/HL/NHLBI NIH HHS; HL-65203/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Endothelial Growth Factors; 0/Intercellular Signaling Peptides and Proteins; 0/Lymphokines; 0/Reactive Oxygen Species; 0/Vascular Endothelial Growth Factor A; 0/Vascular Endothelial Growth Factors |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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