INVESTIGATION OF THE RENAL INJURY CAUSED BY LIVER ISCHEMIA-REPERFUSION IN RATS

To explain the mechanism of renal injury caused by liver ischemia-repe rfusion, we investigated biochemical and morphological changes in the liver and kidney in rats. After reperfusion following 60 min of liver ischemia, numerous changes were found. The level of serum transaminase s and lipid peroxide formation in the liver tissue increased significa ntly. Electron microscopic studies revealed that most of the hepatocyt es had swollen mitochondria and clumping of the nuclear chromatin. The sinusoidal endothelium was disrupted and the sinusoidal lumen was fil led with numerous erythrocytes. Blood endotoxin concentration, plasma lipid peroxide levels, and serum beta-glucuronidase activities were si gnificantly higher than in the control group. Biochemical and morpholo gical renal injury was also observed. Tissue lipid peroxide levels inc reased in both the kidney and the liver. Microscopic examination revea led damage to the renal tubules, including interstitial edema, dilatat ion of the lumen, and granular casts derived from necrotic cells in th e proximal convoluted tubule. The levels of urinary N-acetyl-beta-D-gl ucosaminidase (NAG) in the liver ischemia-reperfusion group were also higher than in the control group. These results suggest that the renal injury was caused by an increase in endotoxin, lipid peroxide, and ly sosomal enzymes in the blood following the liver injury induced by the ischemia-reperfusion.