thioacetamide and Ischemia

We studied the influence of intermittent ischemic injury on thioacetamide-induced liver cirrhosis in rats. Wistar rats were divided into group A, intermittent ischemic injury to liver cirrhosis, and group B, continuous ischemic injury to liver cirrhosis. Total ischemic time was 60 min in both groups. In group A, ischemic injury consisted of a repetition 4 times of 15 min ischemia and 5 min reperfusion. The ATP level of the liver was measured before ischemia, before reperfusion, and 60 min after reperfusion. Bile was collected to determine bile flow rate. The ATP level in the liver tissue 60 min after reperfusion was significantly (p < 0.05) higher in group A than in group B. The ATP level immediately before reperfusion was also significantly (p < 0.05) higher in group A than in group B. The survival rate 1 week after ischemic injury and bile flow rate 60 min after reperfusion were significantly (p < 0.01) higher in group A compared with those in group B. The energy level was much higher in intermittent ischemic injury than in continuous ischemic injury immediately before reperfusion and after reperfusion. Survival rate and bile flow rate were higher in intermittent ischemic injury than in continuous ischemic injury. Therefore it suggests that the viability of the liver was maintained better in intermittent ischemic injury than in continuous ischemic injury.

Topics: Adenosine Triphosphate; Animals; Bile; Ischemia; Liver; Liver Circulation; Liver Cirrhosis, Experimental; Male; Rats; Rats, Wistar; Survival Analysis; Thioacetamide

In order to prevent massive bleeding at hepatectomy, the temporary arrest of hepatic circulation is often performed but it is not clear whether this arrest of circulation is tolerated equally by the cirrhotic liver and the normal liver. We investigated biochemically the detailed effects of ischemia on cirrhotic livers in rats with experimentally induced liver cirrhosis. Thioacetoamide was used to prepare the rat cirrhotic liver model (LC group, n = 6). After laparotomy, the vessels to the left lateral lobe were clamped for 30 min and then declamped. Changes in AST isozymes and the aminogram in the blood were examined after ischemia. Postischemic changes in hepatic adenine nucleotides (AdN) and the brain aminogram were also examined. These were compared with those of normal liver ischemia (N group, n = 6) at 24 hr after recirculation. In the LC group, serum levels of mitochondrial AST, a parameter of necrotic cells, were significantly higher than those of the N group. Hepatic AdN levels decreased to 60.6% of the original levels after ischemic injury but those of the N group remained at 95.4% of the original level. Since AdN in tissue is accepted as a reliable parameter of viable cells, cirrhotic livers subjected to ischemia might have more necrotic cells than normal livers. Sequential analysis of serum aminograms of the LC group after ischemia revealed that the ratio of Val+Leu+Ileu/Tyr+Phe decreased to near 1.0 but that of the N group always remained higher than 3.0. Based on these results, it was concluded that ischemic injury in cirrhotic livers is more hazardous than that in normal livers.

Topics: Adenosine Triphosphate; Amino Acids; Animals; Aspartate Aminotransferases; Brain; Electroencephalography; Energy Metabolism; Ischemia; Isoenzymes; Liver; Liver Cirrhosis, Experimental; Male; Motor Activity; Rats; Reperfusion Injury; Thioacetamide