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作 者:潘娟娟[1] 王卫群[1] 龚辉[1] 范卫[1] 余竹元[2] 申捷[1]
机构地区:[1]复旦大学附属金山医院心内科,上海200540 [2]复旦大学附属中山医院免疫室,上海200032
出 处:《中国临床医学》2009年第4期501-503,共3页Chinese Journal of Clinical Medicine
摘 要:目的:评价妊娠期缺氧对子代成年后心肌缺血再灌注损伤的作用。方法:在SD雌鼠妊娠期第15~21天给予氧浓度10.5%的低氧环境,建立妊娠期缺氧动物模型。缺氧组和对照组子代雄鼠同等条件下饲养至3个月龄作为实验用动物。建立离体鼠Langendorff模型,分别记录缺氧组和对照组模型平衡15min后和缺血30min后再灌注1h内心脏机械功能变化和冠脉流量,测定再灌注1h冠脉流出液一氧化氮合酶(NOS)、内皮型一氧化氮合酶(eNOS)活性,计算梗死心肌占整个左心室质量的比例。结果:建立模型15min后,对照组和缺氧组的基础心脏机械功能和冠脉流量均无显著差异,但缺血再灌注后缺氧组心脏机械功能和冠脉流量的恢复均明显低于对照组。再灌注冠脉流出液中缺氧组NOS和eNOS活性均显著低于对照组。缺氧组心肌梗死面积明显大于对照组。结论:妊娠期缺氧可加重成年后离体心肌缺血再灌注损伤,其作用机制与eNOS活性下降有关。Objective:To investigate the effects of prenatal hypoxia on myocardial ischemia-reperfusion injury. Methods: Timedated pregnant Sprague-Dawley rats were randomly divided into the control group and the hypoxie exposure group (10.5% oxygen from day 15 to 21 of gestation). The male offspring were raised in the same surrounding. At 3 months of age, hearts were isolated and perfused in a modified Langendorff apparatus. The ventricular function was assessed by measuring the left ventricular functional parameters and coronary flow. After baseline recording, hearts were subjected to 30min of global isehemia and lh of reperfusion. The left ventrieular functional parameters, coronary flow, the LV infarct size and nitric oxide synthase activ- ity were assessed. Results:The left ventricular functional parameters and coronary flow were not different between the control group and the hypoxie exposure group. But after ischemia-reperfusion injury, the left ventricular functional parameters, coronary flow, the LV infarct size and nitric oxide synthase activity were significantly worse in hypoxic exposure group than in the control group. Conclusion: Prenatal hypoxia can increase the susceptibility of adult rat heart to ischemia- reperfusion injury, and eNOS plays an important role.
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