title: Impact of mouse strain differences in innate hindlimb collateral vasculature.
abstract: OBJECTIVE
  To assess the importance of genetic background for collateral artery development.
  
  
  RESULTS
  C57BL/6, BALB/c and 129S2/Sv mice were studied after femoral artery ligation by laser Doppler imaging, visible light oximetry, time-of-flight-magnetic resonance imaging, and treadmill testing; C57BL/6 and BALB/c also underwent electron paramagnetic resonance (EPR) oximetry, x-ray angiography, and histology. C57BL/6 had the least initial distal ischemia and most complete recovery. BALB/c had the most severe initial ischemia and poorest recovery. BALB/c had some vasodilatory reserve in their ligated limbs not seen in the other strains at 3 weeks. By in vivo TOF-magnetic resonance angiography, C57BL/6 had larger preexistent and developed collaterals. By x-ray angiography, C57BL/6 had a higher collateral-dependent filling score and number of visible collaterals immediately after femoral ligation and a higher number of visible collaterals at 1 week but not at 4 weeks. EPR oximetry and histology revealed hypoxia and tissue damage in regions of collateral growth of BALB/c but not C57BL/6 mice. In C57BL/6 BrdUrd uptake in the thigh was limited to larger vessels and isolated perivascular cells. Proliferative activity in collateral arterioles was similar in both strains.
  
  
  CONCLUSIONS
  Genetic differences in preexistent collateral vasculature can profoundly affect outcome and milieu for compensatory collateral artery growth after femoral artery occlusion.
authors.affiliation: Department of Experimental Cardiology, Max-Planck-Institute for Physiological & Clinical Research, Bad Nauheim, Germany. Armin.Helisch@dartmouth.edu
authors.forename: Armin
authors.initials: A
authors.lastname: Helisch
authors.forename: Shawn
authors.initials: S
authors.lastname: Wagner
authors.forename: Nadeem
authors.initials: N
authors.lastname: Khan
authors.forename: Mary
authors.initials: M
authors.lastname: Drinane
authors.forename: Swen
authors.initials: S
authors.lastname: Wolfram
authors.forename: Matthias
authors.initials: M
authors.lastname: Heil
authors.forename: Tibor
authors.initials: T
authors.lastname: Ziegelhoeffer
authors.forename: Ulrike
authors.initials: U
authors.lastname: Brandt
authors.forename: Justin D
authors.initials: JD
authors.lastname: Pearlman
authors.forename: Harold M
authors.initials: HM
authors.lastname: Swartz
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Schaper
mesh_terms: D000818:Animals; D004195:Disease Models, Animal; D004578:Electron Spin Resonance Spectroscopy; D005263:Femoral Artery; D006614:Hindlimb / Q000098:blood supply; D006940:Hyperemia / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D007511:Ischemia / Q000235:genetics* / Q000473:pathology / Q000503:physiopathology; D008026:Ligation; D018810:Magnetic Resonance Angiography; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D018482:Muscle, Skeletal / Q000098:blood supply / Q000473:pathology; D018919:Neovascularization, Physiologic / Q000235:genetics*; D009929:Organ Size; D010092:Oximetry; D010108:Oxyhemoglobins / Q000378:metabolism; D013045:Species Specificity
chemical_list: D010108:Oxyhemoglobins