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          Institute: MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut)     Collection: Publikationen des W. G. Kerckhoff-Instituts     Display Documents

ID: 313322.0, MPI für Herz- und Lungenforschung (W. G. Kerckhoff Institut) / Publikationen des W. G. Kerckhoff-Instituts
The range of adaptation by collateral vessels after femoral artery occlusion
Authors:Eitenmuller, I.; Volger, O.; Kluge, A.; Troidl, K.; Barancik, M.; Cai, W. J.; Heil, M.; Pipp, F.; Fischer, S.; Horrevoets, A. J.; Schmitz-Rixen, T.; Schaper, W.
Date of Publication (YYYY-MM-DD):2006-09-15
Title of Journal:Circ Res
Journal Abbrev.:Circ Res
Issue / Number:6
Start Page:656
End Page:662
Audience:Not Specified
Abstract / Description: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.
Free Keywords:*Adaptation, Physiological Animals 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 Rabbits Regional Blood Flow Stress, Mechanical Up-Regulation/genetics rho GTP-Binding Proteins/genetics
External Publication Status:published
Document Type:Article
Communicated by:N. N.
Affiliations:MPI für physiologische und klinische Forschung
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