Published online before print August 24, 2006, doi: 10.1161/01.RES.0000242560.77512.dd
© 2006 American Heart Association, Inc.
Integrative Physiology |
The Range of Adaptation by Collateral Vessels After Femoral Artery Occlusion
From the Max-Planck-Institute for Heart and Lung Research (I.E., K.T., M.H., F.P., W.S.), Bad Nauheim, Germany; Department of Medical Biochemistry, Academic Medical Centre (O.V., A.J.G.H.), University of Amsterdam, The Netherlands; Kerckhoff Clinic (A.K.), Bad Nauheim, Germany; Division of Vascular and Endovascular Surgery (T.S.), Goethe-University of Frankfurt/Main, Germany; Slovak Academy of Sciences (M.B.), Bratislava, Slovakia; Department of Anatomy, Xiangsha School of Medicine (W.C.), Central South University, Xiangsha, Hunan, P.R. China; Department of Medical Biochemistry (S.F.), Liebig-University Giessen, Germany.
Correspondence to Wolfgang Schaper, Max-Planck-Institute for Heart and Lung Research, Arteriogenesis Research Group, Parkstr. 1, D-61231 Bad Nauheim, Germany. E-mailw.schaper{at}kerckhoff.mpg.de
Natural adaptation to femoral artery occlusion in animals by collateral artery growth restores only 
35% of adenosine-recruitable maximal conductance (Cmax) 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. Cmax reached 100% already at day 7 and had, after 4 weeks, surpassed (2-fold) the Cmax 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.
Key Words: arteriogenesis • fluid shear stress • shunt • growth factors • microarrays
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