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大鼠心肺复苏后肺组织的损伤及其影响因素

Mechanism of lung injury after cardiopulmonary resuscitation in rats

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【作者】 李瑞东杨兴易顾桂国

【Author】 LI Rui-Dong 1,YANG Xing-Yi 1* ,GU Gui-Guo 2 (1. Department of Emergency,People’s Hospital of Changzheng Hospital,Second Military Medical University,Critical Care Medicine Center of PLA,Shanghai 200003,China;2. Department of Emergency,People’s Hospital of Pudong New Area,Shanghai 201200)

【机构】 第二军医大学长征医院急救科解放军急救医学中心上海市浦东新区人民医院急诊科 上海200003上海200003上海201200

【摘要】 目的 :研究心肺复苏后大鼠肺组织细胞的损伤及其可能的影响因素。 方法 :选择健康 SD雄性大鼠 16只 ,随机均分为对照组和复苏组 ,采用琥珀酰胆碱 (0 .15 mg/ 10 0 g)窒息合并冰氯化钾 (0 .5 mol/ L,0 .12 ml/ 10 0 g,4℃ )致大鼠心跳骤停 ,停跳 5 min后开始心肺复苏 ,制备大鼠呼吸心跳骤停 -心肺复苏模型。复苏后 3h取动脉血行血气分析 ,取静脉血离心采用放射免疫法测定血清中 TNF- α含量 ,取肺组织测定湿干质量比值 (W/ D)、髓过氧化酶 (MPO)活性和丙二醛 (MDA)含量 ,通过光镜和电镜观察肺组织细胞结构的变化。 结果 :心肺复苏后 3h较对照组大鼠肺 W/ D值明显升高 (P<0 .0 5 ) ,Pa O2 降低 ,血清中 TNF- α含量、肺组织 MDA含量和 MPO活性明显升高 (P<0 .0 5 ) ,光镜、电镜观察结果显示肺组织细胞结构均有较明显受损的征象。结论 :心肺复苏后早期大鼠存在肺组织细胞损伤 ,肺功能受损 ,血清 TNF-α升高 ,氧自由基生成增多 ,中性粒细胞(PMN)在肺组织聚集可能参与了复苏后肺组织细胞损伤的过程。

【Abstract】 Objective:To investigate the mechanism of lung injury after cardiopulmonary resuscitation(CPR) in rats. Methods: Cardiac arrest was induced by asphyxiation(succinylcholine) and ice-cold 0.5 mol/L KCl in rats and CPR was carried out 5 min after arrest. Sixteen adult male Sprague-Dawley rats were randomly allocated into 2 groups:control group(n=8) and CPR group(n=8). The blood gas analysis,serum level of tumor necrosis factor α(TNF-α),lung tissue wet mass/dry mass ratio(W/D),lung malondialde-hyde(MDA) content and myeloperoxidase(MPO) activities were measured 3 h after CPR. The histological appearances of the lungs were observed under light and electron microscope. Results: Compared to the control group,the lung W/D,serum TNF-α,pulmonary MDA and MPO activity increased dramatically in CPR group while PaO 2 decreased 3 h after resuscitation(P<0.05). Histological examination demonstrated the injuries of lung tissues and the changes of the ultrastructure after resuscitation. Conclusion: Although pulmonary dysfunction is not serious,there are pulmonary pathological and ultrastructure damages in the earlier period after CPR. The elevation of TNF-α in systemic circulation,increase of oxygen-derived free radicals and accumulation of pulmonary PMN may play important roles in pulmonary damage after CPR.

【基金】 上海市科技发展基金攻关计划 ( 0 0 11190 19)
  • 【文献出处】 第二军医大学学报 ,Academic Journal of Second Military Medical University , 编辑部邮箱 ,2004年11期
  • 【分类号】R363
  • 【被引频次】9
  • 【下载频次】153
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