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丁苯酞对窒息性心脏骤停大鼠早期心肺复苏的影响
引用本文:郑艳安,赵春香,王瑞刚,张磊,王鹏宇,王林.丁苯酞对窒息性心脏骤停大鼠早期心肺复苏的影响[J].蚌埠医学院学报,2017,42(9).
作者姓名:郑艳安  赵春香  王瑞刚  张磊  王鹏宇  王林
作者单位:河北联合大学附属医院NICU,河北 唐山,063000;河北省高碑店市医院 医保科,074000
基金项目:河北省卫计委重点科技研究计划
摘    要:目的:探讨丁苯酞对窒息性心脏骤停大鼠早期心肺复苏的影响.方法:健康SD大鼠153,采用随机数字表法分为假手术组、心脏骤停复苏组、丁苯酞干预组,各53.监测各组大鼠血流动力学指标,采用免疫组织化学法检测炎症因子,采用流式细胞仪检测相关因子.结果:3组大鼠自主循环恢复后,随时间推移,心率、平均动脉压均呈现出明显增加态势(P<0.05~P<0.01),实验中不同时间点心率与平均动脉压增加幅度均为丁苯酞干预组>心脏骤停复苏组>假手术组(P<0.05~P<0.01).3组大鼠实验20 min时肿瘤坏死因子α、白细胞介素-6、细胞黏附因子-1均较实验前增加(P<0.05),白细胞介素-10、超氧化物歧化酶均较实验前降低(P<0.05);实验20 min时肿瘤坏死因子α、白细胞介素-6和细胞黏附因子-1均为假手术组大鼠>心脏骤停复苏组>丁苯酞干预组(P<0.01);实验20 min时白细胞介素-10和超氧化物歧化酶为丁苯酞干预组>心脏骤停复苏组>假手术组(P<0.05~P<0.01).结论:对窒息性心脏骤停大鼠实施早期心肺复苏时,丁苯酞可改善血流动力学指标,减轻炎症反应,能提高超氧化物歧化酶活性,抑制细胞黏附因子-1表达.

关 键 词:心脏骤停  窒息  丁苯酞  心肺复苏

Effect of butylphthalide on early cardiopulmonary resuscitation in asphyxia cardiac arrest rats
ZHENG Yan-an,ZHAO Chun-xiang,WANG Rui-gang,ZHANG Lei,WANG Peng-yu,WANG Lin.Effect of butylphthalide on early cardiopulmonary resuscitation in asphyxia cardiac arrest rats[J].Journal of Bengbu Medical College,2017,42(9).
Authors:ZHENG Yan-an  ZHAO Chun-xiang  WANG Rui-gang  ZHANG Lei  WANG Peng-yu  WANG Lin
Abstract:Objective:To investigate the effects of butylphthalide on early cardiopulmonary resuscitation in asphyxia cardiac arrest rats. Methods:Fifteen healthy SD rats were divided into the sham group, cardiopulmonary resuscitation group and butylphthalide intervention group using random number table method ( 5 rats each group ) . The hemodynamic parameters were monitored, the inflammatory factors were detected suing immunohistochemistry,and the correlate factors were detected using flow cytometry. Results:After spontaneous circulation recovery in 3 groups,with the time passing,the heart rate and mean arterial pressure gradually increased (P<0. 05 to P<0. 01). The increasing degrees of the heart rate and mean arterial pressure in butylphthalide intervention group were higher than those in cardiopulmonary resuscitation group, and the increasing degrees of the heart rate and mean arterial pressure in cardiopulmonary resuscitation group were higher than those in sham group(P<0. 05 to P<0. 01). Compared with before experiment, the levels of the tumor necrosis factorα,interleukin-6 and cell adhesion factor-1 increased(P<0. 05),while the levels of interleukin-10 and SOD decreased in three groups at 20 min of experiment(P<0. 05). At 20 min of experiment,the levels of tumor necrosis factorα, interleukin-6 and cell adhesion factor-1 in sham group were more than those in cardiopulmonary resuscitation group,and the levels of tumor necrosis factor α, interleukin-6 and cell adhesion factor-1 in cardiopulmonary resuscitation group were more than those in butylphthalide intervention group(P < 0. 01). At 20 min of experiment,the levels of interleukin-10 and SOD in butylphthalide intervention group were more than those in cardiopulmonary resuscitation group, and the levels of interleukin-10 and SOD in cardiopulmonary resuscitation group were more than those in sham group(P <0. 05 to P <0. 01). Conclusions:During the early cardiopulmonary resuscitation in asphyxia cardiac arrest rats, the butylphthalide can improve hemodynamics, reduce inflammation reaction,increase SOD activity and inhibit the expression of cell adhesion factor-1.
Keywords:cardiac arrest  asphyxia  butylphthalide  cardiopulmonary resuscitation
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