摘要
目的:探讨肝脏缺血—再灌注损伤的机制。方法:将健康Wistar大鼠30只,随机分成二组:假手术组(Controlgroup),缺血—再灌注组(I-R group)。假手术组结扎肝镰状韧带,钝性游离左、中叶肝蒂,不作结扎。缺血—再灌注组,用无损伤动脉夹夹闭左、中叶肝蒂,缺血1h,再灌注1h,制成部分(70%)缺血—再灌注模型。用荧光染料罗丹明(Rh123)和碘化丙啶(PI)标记肝细胞,流式细胞仪(FCM)测定线粒体膜电位(ΔΨm),表示为Rh123+PI-细胞和Rh123-PI-细胞所占的百分数。结果:缺血—再灌注后,假手术组大鼠Rh123+PI-细胞占(94.2±2.8)%,Rh123-PI-细胞占(3.9±0.9)%。缺血—再灌注组肝细胞ΔΨm降低,Rh123-PI-细胞(14.1±2.1)%,与假手术组相比明显增多(P<0.01),Rh123+PI-细胞占(83.3±3.9)%,与假手术组相比明显减少(P<0.01)。结论:线粒体膜电位的变化介导了肝脏缺血—再灌注损伤的机制。
Objective： To study the mechanism of heptic ischemia -- reperfusion injury. Method：30 Wistar rats of Medical fitness were divided into two groups at random： false surgery group（ Control group） and ischemia- reperfusion injury group（I- P group）. Broad ligament of liver of rats in control group were deligated, hepatic pedicle of left and middle lobe were spiked with finger and not deligated. Hepatic pedicle of left and middle lobe of all of rats in I - P group were occlused 1 hour by bulldog clamp, then unclamp 1 hour, partialischemia- repeffusion injury model （70%） were made by this way. Heptic cell was marked in fluorochrome rhodamine （Rh123） and propidium iodinate （PI）, Mitochondrial membrane potential （△ψm） was measured by flow cytometry （FCM）, percentage of Rh123 T＋ PI^- cell and Rh123^- PI^- cell was regarded as Mitochondrial membrane potential （△ψm）. Result： After ischemia- reperfusion injury , the percentage of Rh123^ ＋ PI^- cell of rats in control group was （94.2 ± 2.8） %, and Rh123^- PI^- cell of rats was （3.9 ± 0.9 ） % ; △ψm of heptic cell in I - P group was degrade, and Rh123^ - PI^- cell was（ 14.1 ± 2.1 ） % and had obviously increased than that of control group （ P 〈 0.01）, Rh123 ^＋ PI^- cell was （83.3 ± 3.9） % and had obviously decreased than that of control group （ P 〈 0.01） .Conclusion： The change of Mitochondrial membranes potential mediates the mechanism of heptie ischemia--reperfusion injury.
出处
《医学理论与实践》
2005年第12期1377-1378,共2页
The Journal of Medical Theory and Practice
关键词
缺血-再灌注
线粒体膜电位
Ischemia- reperfusion injury, Mitochondrial membrane potential
