Mechanisms of hepatocytic mitochondria damage following septic shock

AIM: To study mechanism of hepatocytic mitochondria damage following septic shock. METHODS: 30 SD rats were randomly divided into three groups: sham operation group, 12 h cecal ligation and puncture (CLP) group and 16 h CLP group. The model of septic shock was made by cecal ligation and puncture. The liver mitochondria respiratory control rate (RCR), phosphate/oxygen (P/O) and ATPase activities were assayed. RESULTS: In 12 h CLP group mean artery pressure (MAP) (9.54±1.26)kPa] was significantly lower than sham operation group (14.58±1.32)kPa,P<0.05]. However, mortality was obviously higher than sham operation group (P<0.05), the liver mitochondria respiratory control rate (1.27±0.25), phosphate/oxygen (1.67±0.34) and Na⁺-K⁺-ATPase (40.80±3.45), Ca²⁺-ATPase (58.00±2.43), Mg²⁺-ATPase (78.30±4.16), Ca²⁺-Mg²⁺-ATPase(2.70±2.25) activities decreased strikingly. The difference between 12 h CLP group and sham operation group was significant (P<0.05), 16 h CLP groups was more lower than 12 h CLP group. As RCR, P/O and ATPase activities were significantly reduced, mortality significantly increased. Futhermore, obvious positive correlation was showed between them (r=0.892,P<0.01;r=0.834,P<0.01). CONCLUSION: Liver mitochondria function of ingestion-oxygen and phosphorus-acidification are decreased and membrane fluxion is weaken. Energy metabolism is blocked and Ca²⁺-Mg²⁺ shows imbalanced. All of them cause hepatocytic mitochondria injury following septic shock.