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四氢生物蝶呤抗幼鼠心肌缺血再灌注损伤的实验研究 被引量:2

Tetrahydrobiopterin reduces immature myocardial ischemic reperfusion injury\
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摘要 目的 观察四氢生物蝶呤(BH4)对未成熟缺血再灌注心肌的保护作用。方法 建立幼鼠离体全心缺血再灌注动物模型,80 只幼鼠随机分为实验组(BH4 停搏液)和对照组(St.ThomasⅡ液),每组40只。测定缺血前、缺血再灌注30min、缺血再灌注60min、缺血再灌注120min时的冠状动脉流出量。取缺血前、缺血30min、缺血再灌注60min时的心肌测定丙二醛(MDA)含量。测定缺血前、缺血30min、缺血再灌注30min、缺血再灌注60min、缺血再灌注120min心肌的一氧化氮(NO)浓度、心肌细胞内核因子κB(NF κB)表达以及心肌细胞间粘附分子1( ICAM 1)的含量。对比研究BH4停搏液与St.ThomasⅡ液的心肌保护效果。结果 在相应时间点,BH4组冠脉流出量的恢复率和心肌NO的浓度均显著高于对照组(P<0.05);而心肌MDA和ICAM -1含量以及心肌细胞内NF -κB的表达均显著低于对照组(P<0.05)。结论 含BH4 心脏停搏液较St.ThomasⅡ液对未成熟心肌具有更好的保护效果。其机制可能与增加NO的产量,抑制心肌细胞NF -κB表达以及降低心肌ICAM- 1的含量有关。 Objective To study the effects of tetrahydrobiopterin (BH4) on immature myocardial ischemia reperfusion injury.Methods The isolated immature rat hearts were perfused in retrograde fashion applying isolated Langendorff model. Eighty immature Wistar rats were divided randomly into two groups(n=40):Control group (St.ThomasⅡ cardioplegic solution) and Test group( BH4 in the St.ThomasⅡ cardioplegia). The hearts in both group were exposed to 30 minutes global ischemia, and then underwent 120 minutes reperfusion. The coronary flow (CF) was recorded before ischemia and after 30, 60, 120 minutes of reperfusion. The myocardial content of malonaldehyde (MDA) was measured at before ischemia and after 30, 60 minutes of reperfusion. The myocardial content of nitrogen monoxide (NO) and intercellular adhesion molecule-1 (ICAM-1), and the levels of myocardial Nuclear factor-kappa B were measured prior to ischemia, post ischemia and after 30, 60, 120 minutes of reperfusion.Results At each time point, the recovery rate of CF and production of myocardial NO in test group were significantly higher than that in control group (P< 0.05) and the myocardial contents of MDA and ICAM-1, and the express level of myocardial Nuclear factor-kappa B in test group were significantly lower than that in control group (P< 0.05).Conclusions BH4 cardioplegia may offer immature myocardial better protection than St.ThomasⅡcardioplegia solution by increasing production of myocardial NO, repressing the level of myocardial Nuclear factor-kappa B, and decreasing the myocardial contents of ICAM-1.
出处 《中华小儿外科杂志》 CSCD 北大核心 2005年第4期207-210,共4页 Chinese Journal of Pediatric Surgery
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参考文献12

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