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目的观察利多卡因对不同载脂蛋白E(apoE)基因型小鼠短暂全脑缺血后脑损害程度的影响。方法健康雄性C57BL/6J野生型小鼠(C57小鼠)和apoE敲除型小鼠(apoE小鼠)随机分为C57对照组(15只,假手术操作),C57缺血组(21只,夹闭双侧颈总动脉17min,经腹腔给予生理盐水),C57利多卡因组(22只,夹闭双侧颈总动脉17min,经腹腔给予利多卡因),apoE对照组(15只,处理同C57对照组),apoE缺血组(19只,处理同C57缺血组),apoE利多卡因组(16只,处理同C57利多卡因组)。术后第7天从各组随机选取小鼠28只进行神经病理检查。其余小鼠从术后第8天起进行Morris水迷宫测试,连续5d。结果(1)海马CA1区缺血神经元百分比分别为C57对照组0.3%±0.1%、C57缺血组19.3%±4.5%、C57利多卡因组36.9%±2.5%、apoE对照组0.6%±0.3%、apoE缺血组65.5%±2.2%、apoE利多卡因组39.4%±6.5%。各缺血组和利多卡因组均明显多于相应的对照组(均P<0.01),C57利多卡因组和apoE缺血组还明显多于C57缺血组(均P<0.01),但apoE利多卡因组明显少于apoE缺血组(P<0.01)。(2)潜伏期除apoE缺血组外,各组均随测试天数增多而明显缩短(P<0.05,0.01)。各缺血组和利多卡因组明显长于相应的对照组(P<0.05,0.01),C57利多卡因组和apoE缺血组还明显长于C57缺血组(P<0.05,0.01),但apoE利多卡因组明显短于C57利多卡因组和apoE缺血组(P<0.05,0.01)。(3)有效搜索策略百分比除C57利多卡因组和apoE缺血组外,各组均随测试天数增多而明显增加(P<0.05,0.01)。各缺血组和利多卡因组明显低于相应的对照组(P<0.05,0.01),C57利多卡因组和apoE缺血组还明显低于C57缺血组(P<0.05,0.01),但apoE利多卡因组明显高于C57利多卡因组和apoE缺血组(P<0.05)。结论短暂全脑缺血导致小鼠明显的脑损害,apoE小鼠脑损害的程度较C57小鼠更重;利多卡因加重了C57小鼠的脑损害,但可减轻apoE小鼠脑损害的程度。
Objective To investigate the effect of lidocaine on the brain damage after transient global cerebral ischemia in mice with different apolipoprotein E (apoE) genotypes. Methods Healthy male C57BL / 6J wild type mice (C57 mice) and apoE knockout mice (apoE mice) were randomly divided into C57 control group (15 sham operation), C57 ischemia group (21 rats, Bilateral common carotid arteries were occluded for 17 min and saline was given intraperitoneally. C57, lidocaine group (n = 22, bilateral common carotid artery occlusion for 17 min, intraperitoneal administration of lidocaine), apoE control group (n = 15) With C57 control group), apoE ischemia group (n = 19, treated with C57 ischemia group), apoE lidocaine group (16 treated with C57 lidocaine group). On the 7th day after surgery, 28 mice were randomly selected from each group for neuropathological examination. The remaining mice were subjected to Morris water maze test from day 8 postoperatively for 5 days. Results (1) The percentages of neurons in CA1 hippocampus were 0.3% ± 0.1% in C57 control group, 19.3% ± 4.5% in C57 ischemia group, 36.9% ± 2.5% in C57 lidocaine group and 0.6% ± in apoE control group 0.3%, 65.5% ± 2.2% in apoE ischemia group and 39.4% ± 6.5% in apoE lidocaine group. There were significantly more ischemic and lidocaine groups than the corresponding control group (all P <0.01), and more in C57-L-icucanine group and apoE-ischemia group than in C57-ischemia group (all P <0.01) The apoE-induced lidocaine group was significantly less than the apoE-ischemia group (P <0.01). (2) In addition to apoE ischemia latency group, each group were significantly shortened as the number of test days increased (P <0.05,0.01). (P <0.05, 0.01). The levels of apoE and apoE were also significantly increased in C57 and C57 groups compared with C57 ischemia group (P <0.05, 0.01) Lidocaine group was significantly shorter than C57 lidocaine group and apoE ischemia group (P <0.05,0.01). (3) The percentage of effective search strategy significantly increased with the increase of test days except for the C57-lidocaine group and the apoE-ischemia group (P <0.05, 0.01). (P <0.05, 0.01), and the levels in ischemic and apoE-ischemic groups were significantly lower than those in C57 ischemic groups (P <0.05, 0.01) However, the apoE lidocaine group was significantly higher than the C57 lidocaine group and apoE ischemia group (P <0.05). CONCLUSION: A transient global cerebral ischemia results in significant brain damage in mice and apoE mice are more brain damaged than C57 mice; lidocaine increases brain damage in C57 mice but decreases brain damage in apoE mice .