Document Detail


Boundary layer infusion of nitric oxide reduces early smooth muscle cell proliferation in the endarterectomized canine artery.
MedLine Citation:
PMID:  9070177     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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.
Authors:
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:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  The Journal of surgical research     Volume:  67     ISSN:  0022-4804     ISO Abbreviation:  J. Surg. Res.     Publication Date:  1997 Jan 
Date Detail:
Created Date:  1997-04-03     Completed Date:  1997-04-03     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  0376340     Medline TA:  J Surg Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  26-32     Citation Subset:  IM    
Affiliation:
Department of Surgery, Veterans Affairs Medical Center, Decatur, Georgia 30033, USA.
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MeSH Terms
Descriptor/Qualifier:
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:
HL 31469/HL/NHLBI NIH HHS; HL 48667/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
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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