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 mumol X g-1 wet weight. Following HAL for 1 h, protein synthesis was reduced to 63% of control value and ATP to 2.4 mumol X 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.(ABSTRACT TRUNCATED AT 250 WORDS)