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目的 盐酸氟桂利嗪对大鼠肝脏缺血／再灌注损伤时肝细胞线粒体的影响。方法 将 Ｗｉｓｔａｒ 大鼠随机分成三组，每组１２ 只。 Ａ组为对照组， Ｂ组缺血／再灌注组， Ｃ组为盐酸氟桂利嗪组。其中 Ｂ， Ｃ两组均阻断肝门造成肝脏完全缺血３０ 分钟后再灌注９０ 分钟。测定各组动物血清中 Ａ Ｌ Ｔ， Ｌ Ｄ Ｈ 含量，肝细胞线粒体脂质过氧化物（ Ｌ Ｐ Ｏ）含量，行超微结构的观察。结果 与 Ａ 组比较， Ｂ组血清 Ａ Ｌ Ｔ， Ｌ Ｄ Ｈ 活性显著增加（ Ａ， Ｂ二组， Ａ Ｌ Ｔ（ Ｉ Ｕ． Ｌ－ １ ）， Ｌ Ｄ Ｈ（ Ｕ． Ｌ－ １）分别为５３．１１±１７．５２，１６８８．９８±２５２．３０， Ｐ＜ ０．０１，１１８８．８８±３８．４７，３５９４．８８±４２８．９４， Ｐ＜ ０．０１）形态学上，肝细胞线粒体发生损伤，肝细胞线粒体脂质过氧化程度（ Ｌ Ｐ Ｏ）增加。 Ａ， Ｂ二组 Ｌ Ｐ Ｏ含量分别为１８．２７±４．６８ｎｍ ｏｌ．１００ｍ ｇ－ １，６５．３０±７．８６ｎｍ ｏｌ．１００ｍ ｇ－ １， Ｐ＜ ０．０１）。与 Ｂ组比较， Ｃ组预用盐酸氟桂利嗪后血清 Ａ Ｌ Ｔ， Ｌ Ｄ Ｈ 活性增高程度降低（７５２．６６±１７１．１０，２３５２．２０±６０１．２０， Ｐ＜ ０．０１），肝细
Effect of Flunarizine Hydrochloride on Hepatocyte Mitochondria in Rat with Hepatic Ischemia / Reperfusion Injury. Methods Wistar rats were randomly divided into three groups of 12 rats. A group as control group, B group ischemia / reperfusion group, C group flunarizine hydrochloride group. Among them, B and C both blocked the hepatic portal and caused the ischemia of the liver for 30 minutes and then the reperfusion for 90 minutes. The levels of A L T and L D H in serum of rats in each group were determined, and the content of L P O in liver cells was measured. The ultrastructure was observed. Results Compared with group A, the activity of serum A L T and L D H in group B was significantly increased (group A and B, A L T (I U. L -1) and L D H (U. L -1) 53.11 ± 17.52,1688.98 ± 252.30, P <0.01,1188.88 ± 38.47,3594.88 ± 428.94, P <0.01) Morphologically, hepatocytes Mitochondria are damaged, and hepatocyte mitochondrial lipid peroxidation (L P O) increases. The contents of L P O in group A and B were 18.27 ± 4.68 nmol respectively. 100 m g - 1,65.30 ± 7.86 nm ol. 100 m g-1, P <0.01). Compared with group B, the increase of serum A L T and L D H activity in group C after pre-treatment with flunarizine hydrochloride was lower (752.66 ± 171.10,2352.20 ± 601.20, P <0.01) Liver fine