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作者采用大鼠盲肠结扎穿孔(CLP)脓毒败血症模型,观察了肾脏线粒体呼吸功能、线粒体膜流动性和线粒体内丙二醛(MDA)含量的变化,各值间做相关分析。CLP12小时,呼吸控制率(RCR)较对照值显著下降(P<0.05),CLP16小时,磷/氧比值(P/O值)也显著下降(P<0.01),至CLP20小时,两值下降更甚,表明脓毒败血症过程中,肾脏线粒体损伤早而严重。CLP过程中,荧光偏振度(P)、各向异性(γ)、微粘度((?))和线粒体内MDA均明显高于对照值(P<0.01),P、MDA与RCR均呈显著负相关,MDA与P呈显著正相关。提示脓毒败血症过程中,线粒体膜流动性下降和线粒体内脂质过氧化损伤是肾线粒体损伤的重要原因。脂质过氧化损伤与线粒体膜流动性下降亦密切相关。
The authors used cecal ligation and puncture (CLP) model of septic sepsis in rats to observe the change of mitochondrial respiratory function, mitochondrial membrane fluidity and the content of malondialdehyde (MDA) in mitochondria. CLP12 hours, respiratory rate (RCR) significantly decreased compared with the control (P <0.05), CLP16 hours, P / O ratio decreased significantly (P <0.01) Very, that sepsis in the process of sepsis, kidney mitochondrial damage early and serious. Fluorescence polarization degree (P), anisotropy (γ), microviscosity (?) And mitochondrial MDA in CLP were significantly higher than those in control (P <0.01), while P, MDA and RCR were significantly negative Correlation, MDA and P was significantly correlated. Prompt sepsis in the process of mitochondrial membrane fluidity decline and mitochondrial lipid peroxidation damage is an important cause of renal mitochondrial damage. Lipid peroxidation and mitochondrial membrane fluidity decline is also closely related.