Changes in calcium content of the liver during hepatic ischemia-reperfusion in dogs

Alteration of calcium metabolism in cells has been thought to be one of the main factors in ischemia-reperfusion injury. Serial changes in the tissue calcium content of the liver and the correlation between calcium level and liver injury were investigated. Experimental dogs were divided into two groups and subjected to hepatic ischemia of different duration: 60 min in Group A and 120 min in Group B, followed by reperfusion. Serum alanine aminotransferase, as an indicator of liver injury, was more elevated in Group B than in Group A. There was no change in hepatic calcium content during ischemia in either group. Immediately after reperfusion, there was no change in hepatic calcium level in Group A, whereas in Group B it was markedly elevated. The peak value occurred 30 min after reperfusion and gradually decreased thereafter, but did not return to pre-ischemic levels during the observation time. Plasma calcium concentrations in hepatic venous blood were markedly decreased in Group B 30 min and 60 min after reperfusion. These results suggest that calcium accumulation in the liver during the early reperfusion period may be one of the mediators of hepatic injury. To elucidate the mechanisms for elevation of calcium in hepatic tissue, serum malondialdehyde, a product of lipid peroxidation, was measured in hepatic venous blood. No elevation of serum malondialdehyde was observed in either group, indicating that the increases in calcium may not be due to oxidative stress. Serum mitochondrial aspartate aminotransferase and electron microscopic findings were used as indicators of mitochondrial injury.(ABSTRACT TRUNCATED AT 250 WORDS)