文章摘要
仇万山,郑 亮,陈亦江,吴延虎,莫绪明,张儒舫.山莨菪碱对体外循环肺损伤的保护作用研究[J].南京医科大学学报,2007,(7):744~747
山莨菪碱对体外循环肺损伤的保护作用研究
The protection research of anisodamine on cardiopulmonary bypass induced lung injury
投稿时间:2006-11-15  
DOI:10.7655
中文关键词: 山莨菪碱  体外循环  肺损伤  保护作用  核因子-κB
英文关键词: anisodamine  cardiopulmonary bypass  lung injury  protection effect  NF-κB.
基金项目:南京医科大学科技发展基金资助项目(NY02051)
作者单位
仇万山 南京医科大学第一附属医院心胸外科,江苏 南京 210029 
郑 亮 南京医科大学第一附属医院心胸外科,江苏 南京 210029 
陈亦江 南京医科大学第一附属医院心胸外科,江苏 南京 210029 
吴延虎 南京医科大学第一附属医院心胸外科,江苏 南京 210029 
莫绪明 南京医科大学附属南京儿童医院心胸外科,江苏 南京 210008 
张儒舫 南京医科大学附属南京儿童医院心胸外科,江苏 南京 210008 
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中文摘要:
      目的:探讨山莨菪碱(654-2)对体外循环肺损伤的保护作用及作用机制?方法: 连续选取24例先心病手术患者,按用药剂量及给药时间不同,随机分成用药Ⅰ组(预充液中加入654-2,2 mg/kg)?Ⅱ组(主肺动脉注入654-2,2 mg/kg)?Ⅲ组(预充液中加入654-2,1 mg/kg;主肺动脉注入654-2,2 mg/kg)与对照组?观测手术过程中5个时间点心房血中炎症细胞数?CD11b水平?TNF-α浓度;术毕肺组织中NF-κB灰度值 ;肺功能的变化?结果:应用山莨菪碱Ⅰ?Ⅱ?Ⅲ组与对照组比较,血中炎症细胞数?CD11b水平?TNF-α;术毕肺组织中NF-κB灰度值均有不同程度降低,且Ⅱ?Ⅲ组较Ⅰ组变化明显,特别是主动脉开放后的D?E点;血气分析结果分析显示,用药Ⅱ组和Ⅲ组的OI 值较其他两组低,而CD 值有明显的升高?结论:山莨菪碱对体外循环肺损伤有一定的保护作用,且从预充液和主肺动脉分别注入的前后嵌合给药途径较好?通过抑制致病因子刺激炎症效应细胞所致的IκB的降解,达到抑制NF-κB活化,是其可能的作用机制?
英文摘要:
      Objective:To study the protective effect and mechanism of anisodamine on cardiopulmonary bypass(CPB) induced lung injury. Methods:According to the medicine dose and administer time,twenty four patients with congenital heart defect (CHD) were divided into four groups. Control group, group Ⅰ(anisodamine 2 mg/kg, priming solution),group Ⅱ(anisodamine 2 mg/kg,main pulmonary artery), group Ⅲ(anisodamine 1mg/kg,priming solution + anisodamine 2 mg/kg,main pulmonary artery). Neutrophil,CD11b and TNF-a were measured at five time points of the operation. Little lung tissue was cut out for detecting NF-κB after the operation. Blood gas analysis were also arranged. Results:The level of neutrophil,CD11b and TNF-α was reduced in group Ⅰ, group Ⅱ and group Ⅲ compared with the control group, especially in group Ⅱ and group Ⅲ. The results of NF-κB was conformity with the former. Certinary blood gas analysis changed better. Conclusion:CPB induced lung injury can be protected with anisodamine, and the gomphosis pathway(administer through priming solution and main pulmonary artery) is better. The protective mechanism may be that anisodamine inhibits the activation of NF-κB.
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