摘要
目的 :探讨败血症休克肝细胞线粒体损伤的机制。方法 :30只SD大鼠随机分为 3组 ,假手术组 ,12h手术组 ,16h手术组。采用盲肠结扎穿孔术 (cecalligationandpuncture)制作败血症休克模型 ,比较手术前后肝细胞线粒体呼吸功能和氧化磷酸化功能的变化及线粒体膜ATP酶的活性改变与大鼠死亡率和血压变化的关系。结果 :12h手术组平均动脉压 (9 5 4± 1 2 6 )kPa明显低于假手术组 (14 5 8± 1 32 )kPa(P <0 0 5 ) ,死亡率明显高于假手术组 (P <0 0 5 ) ,12h手术组肝细胞线粒体Ⅲ态 (1 2 8± 0 2 5 )、P/O比值 (1 6 7± 0 34)、呼吸控制率 (1 2 7± 0 2 5 )、线粒体膜Ca2 + -ATP酶 (5 8 0 0± 2 4 3)、Na+ -K+ -ATP酶 (4 0 80± 3 4 5 )、Mg2 + -ATP酶 (78 30± 4 16 )、Ca2 + -Mg2 + -ATP酶 (2 70± 2 2 5 )活性与假手术组相比较 ,具有显著差异 (P <0 0 5 )。术后 16h组更低于 12h组 ,与大鼠死亡率增加呈显著正相关。结论 :肝细胞线粒体摄氧功能和氧化磷酸化功能减弱 ,膜流动性降低 ,能量代谢功能障碍 。
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), Ca^(2+)-ATPase (58.00±2.43), Mg^(2+)-ATPase (78.30±4.16), Ca^(2+)-Mg^(2+)-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 Ca^(2+)-Mg^(2+) shows imbalanced. All of them cause hepatocytic mitochondria injury following septic shock. [
出处
《中国病理生理杂志》
CAS
CSCD
北大核心
2004年第11期2110-2113,共4页
Chinese Journal of Pathophysiology
基金
湖北省教育厅资助项目 (2 0 0 0B14 0 0 6 )
关键词
休克
脓毒性
肝
线粒体
呼吸控制率
腺苷三磷酸酶
Shock, septic
Liver
Mitochondria
Respiratory control rate
Adenosinetriphosphatase
