BACKGROUND: Mitochondrial respiratory activity is associated with hepatic ischemia/reperfusion injury. AIM: To determine in vitro whether hepatic ischemia/reperfusion injury may be detected regardless mitochondrial respiratory activity. MATERIAL AND METHODS: Twenty-four heartworm-free mongrel dogs of either sex were randomized in the following groups: control, sham-operated dogs; I60, dogs subjected to 60 min of liver ischemia; I30/R60, dogs subjected to 30 min of ischemia e 60 min of reperfusion of liver; I45/R120 animals subjected to 45 min of ischemia and 120 min of reperfusion of liver. Blood and liver samples were taken after surgery to be processed. Mitochondrial respiratory activity was measured with a Clark-type oxygen electrode and mitochondrial membrane potential was calculated. lactic dehydrogenase, aspartate amino transferase and alanine aminotrasferase activities were determinated using laboratory kits, and malondialdehyde content in liver samples was estimated. RESULTS: The group I45/R120 showed increases of serum aminotransferase, lactic dehydrogenase and malondialdehyde in liver samples. Whereas no changes were registered in mitochondrial respiratory activities and mitochondrial membrane potential, a tendency of decrease in the rate of active respiration (state 3) could be observed. CONCLUSION: Under the conditions of this study, the results suggest the data from mitochondrial respiratory activity could show no significance difference among groups in hepatic ischemia/reperfusion injury. Hepatic ischemia reperfusion injury can be detected regardless mitochondrial respiratory activity.
Mitochondria; liver; Reperfusion injury; Oxidative phosphorylation; Liver
