Changes of Protein Synthesis in Liver Tissue following Ligation of Hepatic Artery or Portal Vein in Rats

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Abstract
The effects of short-term (1 h) complete liver ischemia, hepatic artery ligation (HAL) and portal vein ligation (PVL) on protein synthesis and ATP in liver tissue were studied in rats. Protein synthesis was measured by determining rate of amino acid incorporation into protein in incubated liver slices and was reduced to 34% of the control value after 1 h of complete liver ischemia. ATP was reduced from 3.2 to 0.28 µmol × g-1 wet weight. Following HAL for 1 h, protein synthesis was reduced to 63% of control value and ATP to 2.4 µmol × g-1 wet weight. No significant changes of protein synthesis or ATP were noticed 1 h after PVL. The results indicate that deprivation of hepatic arterial blood plays a greater role than exclusion of portal blood for impairment of protein synthesis in short-lasting liver ischemia. The effect of complete ischemia was more pronounced than the sum effect of HAL and PVL, suggesting that accumulation of metabolites and tissue acidosis might contribute to the consequences of abolished blood supply in liver ischemia. In another series of experiments the effects of HAL and PVL on protein synthesis and ATP in liver tissue were studied after 1, 3 and 7 days. Protein synthesis was reduced 1 day after HAL but normalized after 3 days, probably reflecting development of collaterals. Following PVL, protein synthesis was reduced after 1 day and remained depressed up to 7 days at which time it was 55% of the control value. ATP in liver tissue was not significantly different from the control value 1 day after HAL of PVL but was slightly reduced 7 days after PVL. Thus, the results demonstrated that hepatic protein synthesis was rapidly reduced after HAL but returned to normal after a few days. The effects of PVL developed more slowly but were more pronounced and protracted. The effects of HAL are probably caused by hypoxia while reduced protein synthesis following PVL might reflect decreased inflow to the liver of other factors of importance for protein synthesis than oxygen, e.g., amino acids and hormones.