Inhalation of carbon monoxide prevents liver injury and inflammation following hind limb ischemia/reperfusion Michael C. Ott * , Jeffrey R. Scott ‡ , Aurelia Bihari ‡ , Amit Badhwar ‡ , Leo E. Otterbein § , Daryl K. Gray * , Kenneth A. Harris † and Richard F. Potter † ,‡ ,1 * Department of General Surgery and † Vascular Surgery, London Health Sciences Centre, London, Ontario, Canada; ‡ The Centre for Critical Illness Research, Lawson Health Research Institute, London, Ontario, Canada; and § Division of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburg School of Medicine, Pittsburgh, Pennsylvania, USA 4 1 Correspondence: Victoria Research Lab, 6th Floor, Rm. A6-105, 800 Commissioners Rd., London, ON, Canada N6A 4G4. E-mail: rpotter@uwo.ca <h3>SPECIFIC AIMS</h3> In our previous studies we showed significant reductions in microvascular perfusion and hepatocellular injury in the liver after a systemic inflammatory response (SIRS) generated by hind limb ischemia/reperfusion (I/R). We have demonstrated that induction of heme oxygenase in the liver during the early stages of SIRS is an important endogenous protective mechanism. In the present study we use inhaled carbon monoxide (CO) at low concentration (250 ppm) to determine whether remote benefits could be realized
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