[Roles of Mac-1, endogenous TNF-alpha, and IFN-gamma in pathogenesis of hepatic warm ischemia-reperfusion injury].
The roles of neutrophil Mac-1 (CD11b/18) adhesion molecule, TNF-alpha and IFN-gamma in hepatic warm ischemia-reperfusion injury (IRI) were investigated with a newly established mouse model. Blood supply to the left lateral and the median lobe of the liver was interrupted with an atraumatic clip for 50 minutes. From 1 hour to 24 hours after reperfusion, TNF-alpha in the ischemic liver tissue was detected. IFN-gamma was not detected in ischemic liver tissue and blood. Pretreatment with anti-mouse Mac-1 monoclonal antibody (mAb) diminished the plasma GPT level, area of necrosis, and number of myeloperoxidase positive cells in ischemic liver lobe at 24 hours after reperfusion. Pretreatment with anti-mouse TNF-alpha or anti-mouse IFN-gamma mAb did not affected any parameters. From these results, Mac-1 was considered to play an important role in a hepatic warm IRI. However, TNF-alpha and IFN-gamma were not considered to play a pivotal role in the pathogenesis of the injury and in the regulation of the neutrophils adhesion via Mac-1.
First Department of Surgery, Hokkaido University School of Medicine, Sapporo, Japan.
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Tamura
D000818:Animals; D007371:Interferon-gamma / Q000502:physiology*; D007511:Ischemia / Q000209:etiology*; D008099:Liver / Q000098:blood supply*; D016177:Macrophage-1 Antigen / Q000502:physiology*; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D015427:Reperfusion Injury / Q000209:etiology*; D014409:Tumor Necrosis Factor-alpha / Q000502:physiology*
D016177:Macrophage-1 Antigen; D014409:Tumor Necrosis Factor-alpha; D007371:Interferon-gamma