| Boundary layer infusion of nitric oxide reduces early smooth muscle cell proliferation in the endarterectomized canine artery. | |
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MedLine Citation:
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PMID: 9070177 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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To evaluate the direct effect of nitric oxide (NO) on vascular smooth muscle cell (SMC) proliferation in vivo, we used an expanded polytetrafluoroethylene (ePTFE)-based local infusion device to deliver an NO donor, proline/NO (PROLI/NO), to the luminal boundary layer of endarterectomized artery and the distal anastomosis of the graft in a canine model. Once delivered to the blood, PROLI/NO releases NO by a mechanism involving pH-dependent decomposition. Six dogs underwent bilateral femoral artery endarterectomies. ePTFE infusion devices, blindly primed with PROLI/NO to one artery or proline to the contralateral vessel, were anastomosed proximal to the injured segments so that each animal served as its own control. PROLI/NO or proline was continuously delivered for 7 days from an osmotic reservoir, through the wall of the graft infusion device. Euthanasia was carried out at 7 days, and the processed specimens were blindly analyzed for SMC proliferation at both graft anastomoses and endarterectomized segments by a bromodeoxyuridine index assay. All dogs survived with no clinical side effects. In comparing the treated and control vessels, NO released from PROLI/NO significantly reduced SMC proliferation by 43% (13.24 +/- 1.24% versus 23.24 +/- 1.01%, P = 0.004) at the distal anastomoses and by 68% (10.58 +/- 1.63% versus 25.17 +/- 3.39%, P = 0.007) at endarterectomized segments. However, there was no significant difference in blood flow measurements between treated and control arteries (56.25 +/- 6.50 ml/min versus 46.50 +/- 3.20 ml/min, P = 0.094). These data demonstrate that local boundary layer infusion of NO released from PROLI/NO significantly reduces SMC proliferation in injured arteries with no effect on regional blood flow. This study suggests a new strategy to inhibit early SMC proliferation in injured arteries and probably to control intimal hyperplastic lesion formation in the manipulated vessels. |
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Authors:
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C Chen; S R Hanson; L K Keefer; J E Saavedra; K M Davies; T C Hutsell; J D Hughes; D N Ku; A B Lumsden |
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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: The Journal of surgical research Volume: 67 ISSN: 0022-4804 ISO Abbreviation: J. Surg. Res. Publication Date: 1997 Jan |
Date Detail:
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Created Date: 1997-04-03 Completed Date: 1997-04-03 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 0376340 Medline TA: J Surg Res Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 26-32 Citation Subset: IM |
Affiliation:
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Department of Surgery, Veterans Affairs Medical Center, Decatur, Georgia 30033, USA. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Anastomosis, Surgical Animals Cell Division / drug effects Dogs Endarterectomy / instrumentation, methods* Femoral Artery / pathology, surgery Male Muscle, Smooth, Vascular / drug effects*, pathology* Nitric Oxide / pharmacology* Polytetrafluoroethylene |
| Grant Support | |
ID/Acronym/Agency:
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HL 31469/HL/NHLBI NIH HHS; HL 48667/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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10102-43-9/Nitric Oxide; 9002-84-0/Polytetrafluoroethylene |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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