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The complement cascade was inactivated in a model of rat liver ischemia with the purpose of studying the role of complement in tissue injury after ischemia and reperfusion. Soluble human complement receptor type 1 (sCRl) was administered either in a single dose of 25 mg/kg or in 2 doses of 50 mg/kg i.v. over 24 hr after vascular occlusion. Sham-operated rats, nontreated rats submitted to liver ischemia, and rats pretreated with cobra venom factor and submitted to liver ischemia were used as controls.This experiment consists of the temporary interruption of arterial and portal blood flow to the left lateral and medial lobes of the liver for 45 min, followed by a 24-hr period of follow-up after reperfusion. Liver blood flow and hemoglobin saturation were recorded for 1 hr after declamping, with statistically significant differences between the experimental groups and the untreated control group, which received liver ischemia (P<0.001). At 24 hr, galactose elimination was assayed as a liver function test; it was significantly better in the sCRl-treated rats when compared with control rats submitted to ischemia (P<0.01). Alanine aminotransferase levels were also significantly lower in the sCRl-treated rats at 6 and 24 hr (P<0.05). Complement activity was reduced to 25% and 12.5% of normal rats with the respective doses of sCRl. Immunoperoxidase stainings for C3 and C9 were performed on liver sections; they showed endothelial deposits of C3 and C9 in the control group subjected to ischemia. Few C3 deposits were present in the sCRl (25 mg/kg)-treated rats, but not in the cobra venom factor or sCRl (50 mg/kg) groups. These results confirm that complement is inactivated by sCRl with amelioration of reperfusion injury in the rat liver.