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机构地区:[1]哈尔滨医科大学附属第二医院麻醉科黑龙江省麻醉与危重病学研究重点实验室,哈尔滨市150086
出 处:《临床麻醉学杂志》2011年第9期912-915,共4页Journal of Clinical Anesthesiology
基 金:国家自然科学基金资助项目(30872450)
摘 要:目的探讨血红素加氧酶-1(HO-1)对心跳骤停复苏大鼠神经功能的影响。方法雄性SD大鼠65只,随机分为四组:心跳骤停复苏组(Ⅰ组,20只)、氯化高铁血红素组(Ⅱ组,20只)、锡原卟啉组(Ⅲ组,20只)和假手术组(Ⅳ组,5只)。Ⅰ组在心跳骤停后进行标准的心肺复苏直至恢复自主循环(ROSC);Ⅱ和Ⅲ组分别在心跳骤停前12 h或1 h经腹腔注射15 mg/kg的氯化高铁血红素或30μmol/kg锡原卟啉Ⅸ,并进行心肺复苏;Ⅳ组不进行窒息心跳骤停。记录心跳骤停复苏各组的复苏参数,于ROSC后4 d对各组进行神经功能缺陷评分(NDS),随后断头取脑,计数海马CA1区存活神经元数、TUNEL阳性细胞数及caspase 3阳性细胞数。结果心跳骤停复苏各组的复苏参数差异无统计学意义。与Ⅳ组比较,Ⅰ、Ⅱ和Ⅲ组NDS评分明显升高(P<0.05);与Ⅰ组比较,Ⅱ组NDS评分显著降低(P<0.05)。海马CA1区染色显示:与Ⅳ组比较,Ⅰ、Ⅱ和Ⅲ组存活神经元数显著减少,TUNEL阳性细胞数和caspase 3阳性细胞数明显增加(P<0.05);与Ⅰ组比较,Ⅱ组TUNEL阳性细胞数和caspase 3阳性细胞数减少(P<0.05)。结论诱导HO-1的表达可改善心跳骤停复苏后大鼠的神经功能,其机制可能与改善海马CA1区神经元的存活,抑制神经元凋亡有关。Objective To investigate the effects of heme oxygenase-1 (HO-1) on neural function in a rat model of asphyxial cardiac arrest and resuscitation. Methods Sixty-five male SD rats were randomly divided into four groups: cardiac arrest group (group I , n= 20), Hemin group (group Ⅱ , n=20), SnPP group (group Ⅲ, n=20) and Sham group (group IV, n=5). Asphyxial cardiac arrest and resuscitation was performed in group Ⅰ , Ⅱ and Ⅲ, rats in group Ⅱand Ⅲ received an intraperitoneal injection of 15 mg/kg heroin 12 h before the cardiac arrest or 30μmol/kg SnPP Ⅸ 1 h before the cardiac arrest, respectively. At 4 d after return of spontaneous circulation (ROSC), neurological deficits scores (NDS) were evaluated, and then rats were sacrificed and the viable neurons, TUNEL-positive neurons and caspase 3 positive neurons in hippocampus CA1 region were examined. Results There was no significant difference in all variables of asphyxial cardiac arrest in group Ⅰ , Ⅱ and Ⅲ. NDS in group Ⅰ , Ⅱ and Ⅲ were significantly increased when compared with group IV(P〈0.05). Compared with group Ⅳ, the number of viable neurons were decreased while the TUNEL-positive neurons and caspase 3-positive neurons were increased in group Ⅰ , Ⅱ and Ⅲ (P 〈0.05). TUNEL-positive neurons and caspase 3-positive neurons were lower in group Ⅱ than in group Ⅰ (P〈0.05). Conclusion Induction of HO-1 expression can improve the neurological function by increasing the number of viable neurons and decreasing neurons apoptosis in hippocampus CA1 region in rats after cardiac arrest and resuscitation.
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