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  • Title: Extended cold preservation of the graft liver enhances neutrophil-mediated pulmonary injury after liver transplantation.
    Author: Shimizu H, Kataoka M, Ohtsuka M, Ito H, Kimura F, Togawa A, Yoshidome H, Kato A, Miyazaki M.
    Journal: Hepatogastroenterology; 2005; 52(64):1172-5. PubMed ID: 16001655.
    Abstract:
    BACKGROUND/AIMS: The precise mechanisms of pulmonary injury after liver transplantation, especially those associated with cold ischemia time, are not yet clear. METHODOLOGY: We histologically evaluated the number of accumulated polymorphonuclear neutrophils (PMNs) in lungs, and pulmonary injury after liver transplantation with varying periods of cold ischemia (1, 6 and 24h in University of Wisconsin solution at 4 degrees C). Pulmonary expression of cytokine-induced neutrophil chemoattractant (CINC) and macrophage inflammatory protein-2 (MIP-2) mRNA were investigated by quantitative reverse-transcription polymerase chain reaction. The levels of tumor necrosis factor-alpha (TNFalpha), which stimulates these chemokine productions, were also monitored after liver transplantation. RESULTS: The accumulated PMN number, and lung edema, quantified by wet to dry weight ratio, significantly increased in the 24-hr cold-ischemia group after 3h of reperfusion, compared with the 1-hr and 6-hr cold-ischemia groups. Both pulmonary MIP-2 and CINC mRNA expression in the 24-hr group were remarkably upregulated at this time. According to the histological examination, pulmonary injury in the 24-hr group was prominent, characterized by interstitial edema, and alveolar hemorrhage. Furthermore, TNF in the hepatic vein was detected only in the 24-hr group. CONCLUSIONS: Cold ischemia time prolongation upregulates pulmonary MIP-2 and CINC expression via hepatic-derived TNFalpha, and promotes PMN accumulation, resulting in increased pulmonary injury after liver transplantation.
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