title: Inhalation of carbon monoxide reduces skeletal muscle injury after hind limb ischemia-reperfusion injury in mice.
abstract: BACKGROUND
  The purpose of this study was to determine if inhaled carbon monoxide (CO) can ameliorate skeletal muscle injury, modulate endogenous heme oxygenase-1 expression, and improve indexes of tissue integrity and inflammation after hind limb ischemia reperfusion.
  
  
  METHODS
  C57BL6 mice inhaling CO (250 ppm) or room air were subjected to 1.5 hours of ischemia followed by limb reperfusion for either 3 or 6 hours (total treatment time, 4.5 or 7.5 h). After the initial period of reperfusion, all mice breathed only room air until 24 hours after the onset of ischemia. Mice were killed at either the end of CO treatment or at 24 hours' reperfusion. Skeletal muscle was subjected to histologic and biochemical analysis.
  
  
  RESULTS
  CO treatment for 7.5 hours protected skeletal muscle from histologic and structural evidence of skeletal muscle injury. Serum and tissue cytokines were reduced significantly (P < .05) in mice treated with CO for 7.5 hours. Tubulin, heme oxygenase, and adenosine triphosphate levels were higher in CO-treated mice.
  
  
  CONCLUSIONS
  Inhaled CO protected muscle from structural injury and energy depletion after ischemia reperfusion.
authors.affiliation: Division of Vascular and Endovascular Surgery, Department of Surgery, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
authors.forename: Rajendra
authors.initials: R
authors.lastname: Patel
authors.forename: Hassan
authors.initials: H
authors.lastname: Albadawi
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Steudel
authors.forename: Faraz F
authors.initials: FF
authors.lastname: Hashmi
authors.forename: Jeanwan
authors.initials: J
authors.lastname: Kang
authors.forename: Hyung-Jin
authors.initials: HJ
authors.lastname: Yoo
authors.forename: Michael T
authors.initials: MT
authors.lastname: Watkins
mesh_terms: D000255:Adenosine Triphosphate / Q000032:analysis / Q000378:metabolism; D000280:Administration, Inhalation; D000704:Analysis of Variance; D000818:Animals; D001784:Blood Gas Analysis; D002248:Carbon Monoxide / Q000008:administration & dosage*; D003598:Cytoskeletal Proteins / Q000032:analysis / Q000378:metabolism; D004195:Disease Models, Animal; D004797:Enzyme-Linked Immunosorbent Assay; D051547:Heme Oxygenase-1 / Q000032:analysis / Q000378:metabolism; D006614:Hindlimb / Q000293:injuries*; D015850:Interleukin-6 / Q000032:analysis / Q000378:metabolism; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018482:Muscle, Skeletal / Q000293:injuries / Q000503:physiopathology*; D011897:Random Allocation; D015427:Reperfusion Injury / Q000517:prevention & control*; D012680:Sensitivity and Specificity
chemical_list: D003598:Cytoskeletal Proteins; D015850:Interleukin-6; D002248:Carbon Monoxide; D000255:Adenosine Triphosphate; D051547:Heme Oxygenase-1