Document Detail

The range of adaptation by collateral vessels after femoral artery occlusion.
MedLine Citation:
PMID:  16931799     Owner:  NLM     Status:  MEDLINE    
Natural adaptation to femoral artery occlusion in animals by collateral artery growth restores only approximately 35% of adenosine-recruitable maximal conductance (C(max)) probably because initially elevated fluid shear stress (FSS) quickly normalizes. We tested the hypothesis whether this deficit can be mended by artificially increasing FSS or whether anatomical restraints prevent complete restitution. We chronically increased FSS by draining the collateral flow directly into the venous system by a side-to-side anastomosis between the distal stump of the occluded femoral artery and the accompanying vein. After reclosure of the shunt collateral flow was measured at maximal vasodilatation. C(max) reached 100% already at day 7 and had, after 4 weeks, surpassed (2-fold) the C(max) of the normal vasculature before occlusion. Expression profiling showed upregulation of members of the Rho-pathway (RhoA, cofilin, focal adhesion kinase, vimentin) and the Rho-antagonist Fasudil markedly inhibited arteriogenesis. The activities of Ras and ERK-1,-2 were markedly increased in collateral vessels of the shunt experiment, and infusions of L-NAME and L-NNA strongly inhibited MAPK activity as well as shunt-induced arteriogenesis. Infusions of the peroxinitrite donor Sin-1 inhibited arteriogenesis. The radical scavengers urate, ebselen, SOD, and catalase had no effect. We conclude that increased FSS can overcome the anatomical restrictions of collateral arteries and is potentially able to completely restore maximal collateral conductance. Increased FSS activates the Ras-ERK-, the Rho-, and the NO- (but not the Akt-) pathway enabling collateral artery growth.
Inka Eitenmüller; Oscar Volger; Alexander Kluge; Kerstin Troidl; Miroslav Barancik; Wei-Jun Cai; Matthias Heil; Frederic Pipp; Silvia Fischer; Anton J G Horrevoets; Thomas Schmitz-Rixen; Wolfgang Schaper
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2006-08-24
Journal Detail:
Title:  Circulation research     Volume:  99     ISSN:  1524-4571     ISO Abbreviation:  Circ. Res.     Publication Date:  2006 Sep 
Date Detail:
Created Date:  2006-09-15     Completed Date:  2006-10-12     Revised Date:  2009-11-19    
Medline Journal Info:
Nlm Unique ID:  0047103     Medline TA:  Circ Res     Country:  United States    
Other Details:
Languages:  eng     Pagination:  656-62     Citation Subset:  IM    
Max-Planck-Institute for Heart and Lung Research, Bad Nauheim, Germany.
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MeSH Terms
Adaptation, Physiological*
Arterial Occlusive Diseases / physiopathology*
Arteries / growth & development
Cells, Cultured
Collateral Circulation / physiology*
Femoral Artery / pathology*
Gene Expression Profiling
Mitogen-Activated Protein Kinases / genetics
Muscle, Smooth, Vascular / cytology
Neovascularization, Physiologic / genetics*
Regional Blood Flow
Stress, Mechanical
Up-Regulation / genetics
rho GTP-Binding Proteins / genetics
Reg. No./Substance:
EC Protein Kinases; EC GTP-Binding Proteins
Comment In:
Circ Res. 2006 Sep 15;99(6):567-9   [PMID:  16973912 ]

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