Article Summary
徐瑞芬1 张国良1 徐浩1 徐礼鲜1 冯旭阳.高氧液预处理对兔心肌缺血再灌注损伤的影响[J].现代生物医学进展英文版,2012,12(1):23-26.
高氧液预处理对兔心肌缺血再灌注损伤的影响
Protective Effects of Hyperoxia Solution Preconditioning on MyocardialIschemica-Reperfusion Injury in Rabbits
  
DOI:
中文关键词: 高氧液  心肌  缺血预处理  再灌注损伤
英文关键词: Hyperoxia solution  Myocardium  Ischemic preconditioning  Reperfusion injury
基金项目:陕西省自然科学基金(2009JM4023);陕西省社发攻关项目(2010k16-04-05);国家自然科学基金(81000597)和(81070248)
Author NameAffiliation
XU Rui-fen, ZHANG Guo-liang, XU Hao, XU Li-xian, FENG Xu-yang△ 第四军医大学口腔医院麻醉科 
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中文摘要:
      目的:研究高氧液预处理对兔心肌缺血再灌注损伤的影响。方法:雄性新西兰白兔32 只,随机分为4 组(n=8), 结扎- 开放冠 状动脉左前降支(LAD)建立心肌缺血再灌注模型。假手术组(Sham 组)只穿线环绕LAD 不结扎;吸氧组(OX 组)结扎前30 min 经鼻吸纯氧2L/ min;在结扎LAD 前30 min 分别静脉注射HO 10 ml / kg (HO1 组)、20 ml / kg (HO2 组)。于结扎LAD 前即刻(T0,基 础值)、开放LAD 前即刻(T1)、再灌注60 min(T2)及再灌注120 min(T3)时记录HR 和MAP,于T3 时抽取动脉血样3 ml, 测定血清 肌酸激酶(CK)、肌钙蛋白I (cTNI)的活性和IL-6 和TNF-α 的浓度,并测定心肌梗死范围。结果:I/S 组与T0 时比较,T 1-3 时各组 HR、MAP 进行性下降( P< 0.05 );三组间HR、MAP 比较差异无统计学意义( P>0.05)。与Sham 组比较,I/S 组血清CK、cTNI、IL-6 和TNF-α 含量明显升高(P 0.01);与OX 组比较,HO2 组上述酶及炎症因子浓度显著下降(P<0.01),心肌梗死范围减小(P< 0.05)。 结论:高氧液预处理可减轻兔心肌缺血再灌注损伤,机制可能与其抑制炎性反应有关。
英文摘要:
      Objective: To invstigate the effect of hyperoxia solusion preconditioning on myocardial ischemica-reperfusion(I/R) injury in rabbits. Methods: Thirty-two adult male rabbits weighing 2-3 kg were randomly divided into 4 groups (n=8 each): sham operation (group S), myocardial (I/R)(group OX), group HO1, HO2 ( received hypoeroxia solusion 10,20 ml/kg respectively at 30 min before myocardial ischemia ). Myocardial I/R was produced by temporary ligation of anterior descending branch of left coronary artery (LAD) for 30 min followed by 120 min reperfusion. Myocardial ischemia was confirmed by S-T segment elevation and change in color of myocardium. HR and BP were monitored and recorded immediately before ligation of LAD (T0), immediately before LAD ligation was untied (T1) , 60 (T2) and 120 (T3) min after LAD was untied. Blood samples were obtained at T3 for determination of serum CK, cTNI, IL-6 and TNF-α- concentration. Results: In group OX, HO1, HO2, HR and MAP decreased during T1-3(P< 0.05), but there was no significant difference among the 3 groups. In I/R group, the s CK, cTNI, IL-6 and TNF-α were significantly higher than that in Sham group(P<0.01); The above parameters in group HO2, were significantly lower and the infarct size was significantly smaller than that in group OX. Conclusion: Hyperoxia solution preconditioning can attenuate myocardial I/R injury by inhibiting inflammatory response.
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