摘要
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。
In this paper,respiratory function,membrane fluidi-ty,and malondialdehyde(MDA)of kidney mitochondriawere observed during cecum ligation and puncture(CLP)sepsis in rats.At 12 h after CLP,respiratorg control rate(RCR)decreased(P<0.05,vs control value).Phospho-rus/oxygen rate(P/O)decreased significantly(P<0.01)at 16 h after CLP.The values of RCR and P/O furtherdecreased at 20 h after CLP.These results showed thatthe injury of kidney mitochondria appeared early and wassevere during pyosepticemia.The values of P,(?),andMDA of mitochondria were higher than the control valuesafter CLP(P<0.01).There was a negative correlationbetween P,MDA and RCR.The value of MDA had apositive correlation with P.These results suggest that thedecrease of membrane fluidity of mitochondria and lipidperoxidation injury in mitochondria may be the maincause of damage to kidney mitochondria,and lipid peroxi-dation injury may have a close relationship with the de-crease of membrane fluidity of mitochondria.
出处
《中国危重病急救医学》
CAS
CSCD
1992年第4期195-198,共4页
Chinese Critical Care Medicine
