| Endothelial nitric oxide synthase affects both early and late collateral arterial adaptation and blood flow recovery after induction of hind limb ischemia in mice. | |
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MedLine Citation:
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PMID: 19879098 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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OBJECTIVE: The goals of this study were to determine if endothelial nitric oxide synthase (eNOS) affects both early and late collateral arterial adaptation and blood flow recovery after severe limb ischemia in a mouse model and to determine if eNOS-derived NO is necessary for recruitment of chemokine (C-X-C motif) receptor 4 (CXCR4)(+) vascular endothelial growth factor receptor-1 (VEGFR1)(+) hemangiocytes to the site of ischemia. METHODS: Two studies were completed. In the first, hind limb ischemia was induced by unilateral femoral artery excision in three groups: C57Bl6 (wild-type), eNOS(-/-), and C57Bl/6 mice treated with N(G)-nitro-L-arginine methyl ester (L-NAME) from 1 day before excision through day 3 after excision (early L-NAME group). These groups were studied on day 3 after induction of ischemia. In the second study, hind limb ischemia was induced in C57Bl/6 mice (wild-type) and C57Bl/6 mice treated with L-NAME from days 3 through 28 after induction of ischemia. These groups were studied day 28 after ischemia induction. Dependent variables included hind limb perfusion, collateral artery diameter, and the number and location of hemangiocytes within the ischemic hind limb. RESULTS: In the first study, toe gangrene developed in the eNOS(-/-) and early L-NAME treatment groups by day 2. These groups demonstrated less blood flow recovery and smaller collateral artery diameter than the wild-type group. Hemangiocytes were present within the adventitia of collateral arteries in the wild-type group but were only sparsely present, in a random pattern, in the eNOS(-/-) and early L-NAME treatment groups. In the second study, the late L-NAME group showed less blood flow recovery and smaller collateral artery diameter on day 28 of ischemia than the wild-type group. Hemangiocytes were present in a pericapillary distribution in the wild-type group, but were present only sparsely in the late L-NAME treatment group. CONCLUSION: Early (day 3) and late (day 28) adaptive responses to hind limb ischemia both require eNOS-derived NO. NO is necessary for normal hemangiocyte recruitment to the ischemic tissue. |
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Authors:
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Brian Park; Ari Hoffman; Yagai Yang; Jinglian Yan; Guodong Tie; Hossein Bagshahi; Philip T Nowicki; Louis M Messina |
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Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural Date: 2009-10-30 |
Journal Detail:
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Title: Journal of vascular surgery : official publication, the Society for Vascular Surgery [and] International Society for Cardiovascular Surgery, North American Chapter Volume: 51 ISSN: 1097-6809 ISO Abbreviation: J. Vasc. Surg. Publication Date: 2010 Jan |
Date Detail:
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Created Date: 2010-02-01 Completed Date: 2010-02-23 Revised Date: 2011-07-19 |
Medline Journal Info:
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Nlm Unique ID: 8407742 Medline TA: J Vasc Surg Country: United States |
Other Details:
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Languages: eng Pagination: 165-73 Citation Subset: IM |
Copyright Information:
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Copyright 2010 Society for Vascular Surgery. Published by Mosby, Inc. All rights reserved. |
Affiliation:
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Division of Vascular Surgery, University of Massachusetts Medical School, Worcester, Mass 01655, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Chemotaxis Collateral Circulation* / drug effects Disease Models, Animal Enzyme Inhibitors / pharmacology Gangrene Hindlimb Ischemia / enzymology*, pathology, physiopathology Mice Mice, Inbred C57BL Mice, Knockout Muscle, Skeletal / blood supply* NG-Nitroarginine Methyl Ester / pharmacology Nitric Oxide / metabolism* Nitric Oxide Synthase Type III / antagonists & inhibitors, deficiency, genetics, metabolism* Receptors, CXCR4 / metabolism Recovery of Function Regional Blood Flow* / drug effects Stem Cells / metabolism Time Factors Toes / pathology Vascular Endothelial Growth Factor Receptor-1 / metabolism |
| Grant Support | |
ID/Acronym/Agency:
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HL75353/HL/NHLBI NIH HHS; R01 HL075353-05/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/CXCR4 protein, mouse; 0/Enzyme Inhibitors; 0/Receptors, CXCR4; 10102-43-9/Nitric Oxide; 50903-99-6/NG-Nitroarginine Methyl Ester; EC 1.14.13.39/Nitric Oxide Synthase Type III; EC 1.14.13.39/Nos3 protein, mouse; EC 2.7.10.1/Vascular Endothelial Growth Factor Receptor-1 |
| Comments/Corrections | |
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