Postischemic liver damage in rats: Amino acid analysis and morphometric studies.

Abstract

Normothermic, temporary, total ischemia of the liver was produced for 60-225 min under transient portal decompression with a bypass between the mesenteric and the femoral vein. Total amino acids in the liver tended to increase after an ischemic period of > 120 min without reperfusion as compared with control with increasing trends in most of the individual amino acids. In a group undergoing 120 min of ischemia and 60 min of reperfusion, total amino acids and individual amino acids tended to decrease. Total plasma amino acids significantly increased after ischemia of > 120 min. Without reperfusion, elevations of almost all amino acids except for branched chain amino acids were found, whereas after reperfusion most of the individual amino acids also increased, including branched chain amino acids. Molar ratios of branched chain amino acids to tyrosine and phenylalanine decreased only after > 120 min ischemia without reperfusion. Volume ratios of organelle disintegration on EM, such as mitochondrial degradation and autophagic vacuoles, were moderately increased after 90 min ischemia with a further steep rise after > 120 min ischemia. The survival rates of the animals after 60, 90 and 120 min ischemia were 35% (6/17), 27% (3/11) and 25% (3/12), respectively. The following conclusions were obtained: Prenecrosis of the hepatocytes with simultaneous protein degradation started after ischemia for .apprx. 2 h. The survival rates of the animals after 60 and 90 min ischemia were very low despite mild necrosis of the liver. Most of the amino acids in the liver were washed out into the plasma to cause an abnormal plasma amino acid pattern in the acute state. However, the molar ratio of branched chain amino acids to aromatic group was not reduced, in contrast to the ischemic group without reperfusion.