The potential mediators involved in ischemia-reperkines and polymorphonuclear leukocytes (PMN) may fusion injury are numerous. 1,2 Acute phase reactant play a critical role in ischemia-reperfusion injury. To cytokines and polymorphonuclear leukocyte (PMN) adevaluate whether similar mechanisms are operative in hesion were found to be critical in the pathogenesis of human liver, six cirrhotic and nine noncirrhotic patients warm ischemic injury in several animal and human undergoing right hepatectomy were randomized for utistudies, including the muscle, 3 lung, 4 and intestine. 5 lization of hepatic vascular exclusion (HVE) as a model To our knowledge, tumor necrosis factor a (TNF-a) is of ischemia-reperfusion injury. Portal and systemic levthe only cytokine that has been examined during heels of acute reactant cytokines (interleukin 6 [IL-6], inpatic warm ischemia, and its role remains controverterleukin 1 [IL-1], tumor necrosis factor a [TNF-a]) and sial. In a 90-minute hepatic warm ischemia model in neutrophil adhesion in serial liver biopsy specimens were studied. Correlations among mediators, leukocyte the rat, Colleti et al. 6 observed significant release of adhesion, and markers of liver injury were also evalu-TNF-a at the time of reperfusion followed by hepatoated. Hepatic vascular exclusion resulted in substantial cyte necrosis and pulmonary capillary leak syndrome. and reproducible changes in portal and arterial IL-6 lev-This suggested that TNF-a might be an important local els in both cirrhotic and noncirrhotic patients. Portal and systemic mediator of injury in liver ischemia. In and systemic cytokine levels were comparable in most contrast, Chazouille `res et al. 7 failed to show any ininstances, whereas levels were usually higher in circrease in TNF-a levels in four liver resection patients rhotic patients than in noncirrhotic patients. Negative with hepatic vascular exclusion (HVE) for a maximum correlations were found between IL-6 levels at the time period of 60 minutes.
of reperfusion and later TNF-a levels. IL-6 levels correlated negatively with numerous markers of hepatocellu-
Temporary HVE is often used to minimize blood loss lar injury and the number of postoperative complicaduring liver resection. 8,9 This procedure results in contions. Hepatic vascular exclusion increased neutrophils trolled liver ischemia with associated local and sysadhesion after reperfusion in cirrhotic patients but not temic effects at the time of ischemia and after reperfuin noncirrhotic patients. In cirrhotic patients, the desion. Few data are available on the effects of HVE on gree of leukocyte adhesion after reperfusion correlated the release of cytokines and the mechanisms of ischewith several postoperative markers of liver injury. This mia-reperfusion injury in this setting. Most human study in humans shows that acute reactant cytokines studies on hepatic warm ischemia have been designed are released during liver ischemia and, interestingly, that IL-6 levels strongly correlate with clinical and labo-to identify the maximum duration of ischemia that a ratory measures of injury. Further studies to evaluate liver can tolerate without providing insights on potenpossible causal relationship with hepatic injury are wartial mechanisms of injury. 8-10 Furthermore, data from ranted, with emphasis on the role of IL-6 and PMN adheliver transplantation studies are difficult to interpret