ALTERATION OF RETICULOENDOTHELIAL PHAGOCYTIC FUNCTION AND TUMOR NECROSIS FACTOR-?? PRODUCTION AFTER TOTAL HEPATIC ISCHEMIA1

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Abstract
This study was conducted to determine whether the duration of total hepatic ischemia influences reticuloendothelial phagocytic activity and tumor necrosis factor (TNF)-alpha production after reperfusion. Male rats pretreated with either normal saline (NS group) or gadolinium chloride (7 mg/kg) for 2 days to inhibit Kupffer cell function (GC group) were subjected to 30, 60, or 90 min of total hepatic ischemia. The animals tolerated hepatic ischemia well for 30 and 60 min. Although the 7-day survival rate of the NS group decreased to 28% after 90 min of hepatic ischemia, that of the GC group improved significantly to 68% (P<0.01). In the NS group, plasma alanine transaminase and TNF-alpha levels after reperfusion increased with the length of hepatic ischemia. The phagocytic index (PI) after 60 min of reperfusion following 90 min of hepatic ischemia showed significant depression compared with the preischemic level and the value after 30 or 60 min of ischemia. The GC group had significantly lower plasma alanine transaminase and TNF-alpha levels as well as significantly less polymorphonuclear leukocyte infiltration in the liver compared with the NS group. The preischemic PI was significantly inhibited in the GC group when compared with that in the NS group, but PI in the GC group did not change significantly after reperfusion, irrespective of the ischemic time. This study demonstrated that warm ischemia of up to 60 min is tolerable for normal rat liver without a detrimental effect on phagocytic activity. Modulation of Kupffer cell function may have the potential to prevent reperfusion injury after hepatic ischemia, which may allow safe prolongation of the ischemic time.