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作 者:刘斌[1] 梁贵友[2] 蔡庆勇[2] 牛义民[2] 王攀[3] 高振宇[4]
机构地区:[1]遵义医学院附属医院小儿普胸泌科,贵州遵义563000 [2]遵义医学院附属医院胸心外科,贵州遵义563000 [3]遵义医学院附属医院同位素科,贵州遵义563000 [4]遵义医学院外科动物实验中心,贵州遵义563000
出 处:《遵义医学院学报》2009年第4期343-345,共3页Journal of Zunyi Medical University
基 金:贵州省科技攻关项目[2007]-1032
摘 要:目的观察罗格列酮对犬体外循环(cardiopulmonary bypass,CPB)缺血再灌注心肌胰岛素抵抗(insulin resistance,IR)中血清肿瘤坏死因子-α(TNF-α)的干预作用。方法12条健康杂种犬,随机分为两组。组Ⅰ(n=6),主动脉阻断120min;组Ⅱ(n=6)主动脉阻断120min并于心脏停搏液中加入罗格列酮(1mg/kg)。分别于转流前、开放主动脉后15、45、75min时采集冠状静脉窦及外周动脉血标本,比较相应时间点血浆葡萄糖、胰岛素、TNF-α浓度及计算心肌葡萄糖净摄取量、胰岛素抵抗指数(IRI)的变化。结果缺血再灌注后血浆葡萄糖、胰岛素及IRI均较转流前不同程度明显增高,于再灌注15min达峰值;同时心肌对葡萄糖的摄取、利用严重障碍。与组Ⅰ比较,组Ⅱ血浆血糖及胰岛素明显减低,并且心肌葡萄糖利用较组Ⅰ有明显改善(P<0.05)。血浆TNF-α于再灌注后浓度明显增加,于再灌注后15min时达到峰值,此后逐渐下降。与组Ⅰ比较,组Ⅱ再灌注后血浆TNF-α明显减低(P<0.05)。结论在心肌停搏液中加入罗格列酮,可以降低血浆TNF-α的浓度,明显减轻CPB期间心肌IR,改善CPB期间心肌缺血再灌注损伤。Objective To observe the intenvention of rosiglitazone against serum tumor necrosis factor-alpha (TNF-α) in myocardial insulin resistance (IR) during eardiopulmonary bypass (CPB) in dogs. Methods In a canine model, myocardial ischemia was induced by cardial pulmonary bypass for 120-min.Rosiglitazone was mixed with cardioplegic solution. The plasma concentrations of insulin,glueose.TNF-α and the change of insulin resistance index (IRI) were measured at prebypass (control),and aortic cross-clamp off (ischemia-reperfusion) at 15,45,and 75min, respectively. Results After myocardial ischemia-reperfusion,the plasma concentrations of glucose.insulin and IRI were significantly increased and reached their peak levels after being repeffused 15 minutes later (P〈0.05);Meanwhile there was severe dysfunction in myocardial glucose uptaking and utilization. Comparied with group Ⅰ ,the increase degree of those indexes was less obvious in group Ⅱ .After ischemia-reperfusion, TNF-α increased obviously and reached peak points after being reperfused 15 minutes Iater. Comparied with group Ⅰ , TNF-α in group 1/ also increased, but to a much lesser extent (P〈0.05). Conclutions Adding rosiglitazone into the cardioplegic solution can decrease the TNF-α and mitigate the myocardial insulin resistance during CPB.
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