| Bradycardia stimulates vascular growth during gradual coronary occlusion. | |
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MedLine Citation:
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PMID: 16051883 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: In cultured endothelium, stretch induces release of growth factors that contribute to angiogenesis. We tested the hypothesis that bradycardia, which prolongs ventricular diastolic filling time and volume, promotes collateral vessel growth. METHODS AND RESULTS: An ameroid occluder was placed on coronary arteries of dogs with normal heart rates (AM) or bradycardia (55 bpm; AM+BC). A third group had normal heart rates and no ameroid (control [CON]). Four weeks after occluder placement, myocardial blood flow at rest and maximal vasodilation (adenosine) at equivalent heart rates and vascular morphometry of hearts were measured. In AM dogs, conductance (myocardial flow/diastolic pressure) of collateral-dependent myocardium was similar to collateral-independent myocardium during rest but increased to only one third of CON during maximal vasodilation. In contrast, in AM+BC dogs, conductance was similar in collateral-dependent and -independent regions during maximal vasodilation. Arteriolar length density in collateral-dependent myocardium was 80% greater in AM+BC than AM dogs. Capillary length density in collateral-dependent region of AM dogs was lower than CON but normal in AM+BC dogs. The angiopoietin receptor Tie-2 increased in collateral-dependent regions of AM and AM+BC groups, whereas vascular endothelial growth factor increased in collateral-dependent and -independent regions only in AM+BC dogs. CONCLUSIONS: Chronic bradycardia during gradual coronary artery occlusion facilitates angiogenesis/arteriogenesis in collateral-dependent myocardium and preserves maximal perfusion. |
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Authors:
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Kathryn G Lamping; Wei Zheng; Dezhi Xing; Lance P Christensen; James Martins; Robert J Tomanek |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. Date: 2005-07-28 |
Journal Detail:
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Title: Arteriosclerosis, thrombosis, and vascular biology Volume: 25 ISSN: 1524-4636 ISO Abbreviation: Arterioscler. Thromb. Vasc. Biol. Publication Date: 2005 Oct |
Date Detail:
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Created Date: 2005-10-03 Completed Date: 2006-01-10 Revised Date: 2009-11-19 |
Medline Journal Info:
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Nlm Unique ID: 9505803 Medline TA: Arterioscler Thromb Vasc Biol Country: United States |
Other Details:
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Languages: eng Pagination: 2122-7 Citation Subset: IM |
Affiliation:
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Department of Internal Medicine, University of Iowa, Roy J. and Lucille A. Carver College of Medicine, Iowa City, IA, USA. kathryn-lamping@uiowa.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Arterioles / physiology Bradycardia / physiopathology* Capillaries / physiology Chronic Disease Coronary Circulation / physiology* Coronary Disease / physiopathology* Coronary Vessels / physiology Diastole / physiology Dogs Neovascularization, Physiologic / physiology* Receptor, TIE-2 / metabolism Up-Regulation Vascular Endothelial Growth Factor A / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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HL 39050/HL/NHLBI NIH HHS; HL62587/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Vascular Endothelial Growth Factor A; EC 2.7.10.1/Receptor, TIE-2 |
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