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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 observe the protective effect of tetrahydrobiopterin (BH4) on immature ischemia-reperfusion myocardium. Methods The isolated rat model of global ischemia / reperfusion was established. Eighty young rats were randomly divided into experimental group (BH4 cardioplegia) and control group (St.Thomas Ⅱ), 40 rats in each group. Coronary artery outflows were measured before ischemia, 30min after ischemia-reperfusion, 60min after ischemia-reperfusion and 120min after ischemia-reperfusion. Before myocardial ischemia, ischemia 30min, myocardial ischemia 60min myocardial MDA content was measured. The levels of nitric oxide (NO), the expression of nuclear factor κB (NF κB) and the expression of NF κB in myocardial cells before ischemia, 30min ischemia, 30min ischemia reperfusion, 60min ischemia reperfusion, 120min ischemia- Adhesion molecule 1 (ICAM 1) content. The myocardial protective effect of BH4 cardioplegia and St.Thomas Ⅱ fluid was compared. Results At the corresponding time points, the recovery rate of coronary outflow and the concentration of myocardial NO in BH4 group were significantly higher than those in control group (P <0.05), while the content of MDA and ICAM-1 in myocardium and the expression of NF-κB in myocardial cells Significantly lower than the control group (P <0.05). Conclusion BH4 cardioplegia has better protective effect on immature myocardium than St.Thomas Ⅱ solution. The mechanism may be related to increasing the production of NO, inhibiting the expression of NF-κB in myocardial cells and decreasing the content of ICAM-1 in myocardium.