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Vitamin C Prevents Intrauterine Programming of in vivo Cardiovascular Dysfunction in the Rat

机译:维生素C防止子宫内编程的大鼠体内心血管功能障碍

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Background: ?Fetal hypoxia is common and in vitro evidence supports its role in the programming of adult cardiovascular dysfunction through the generation of oxidative stress. Whether fetal chronic hypoxia programmes alterations in cardiovascular control in vivo, and if these alterations can be prevented by antioxidant treatment, is unknown. This study investigated the effects of prenatal fetal hypoxia, with and without maternal supplementation with vitamin C, on basal and stimulated cardiovascular function in vivo in the adult offspring at 4 months of age in the rat. Methods and Results: ?From days 6 to 20 of pregnancy, Wistar rats were subjected to Normoxia, Hypoxia (13% O2), Hypoxia+Vitamin C (5mg/ml in drinking water) or Normoxia+Vitamin C. At 4 months, male offspring were instrumented under urethane anaesthesia. Basal mean arterial blood pressure, heart rate and heart rate variability (HRV) were assessed, and stimulated baroreflex curves were generated with phenylephrine and sodium nitroprusside. Chronic fetal hypoxia increased the LF/HF HRV ratio and baroreflex gain, effects prevented by vitamin C administration during pregnancy. Conclusions: ?Chronic intrauterine hypoxia programmes cardiovascular dysfunction in vivo in adult rat offspring; effects ameliorated by maternal treatment with vitamin C. The data support a role for fetal chronic hypoxia programming cardiovascular dysfunction in the adult rat offspring in vivo through the generation of oxidative stress in utero.??( Circ J ?2013; 77: 2604–2611)
机译:背景:胎儿缺氧很普遍,体外证据通过氧化应激的产生支持其在成人心血管功能障碍的编程中的作用。胎儿慢性低氧是否能在体内控制心血管控制的改变,以及是否可以通过抗氧化剂治疗防止这些改变,目前尚不清楚。这项研究调查了有或没有母体补充维生素C的产前胎儿低氧对大鼠4个月大后代体内基础和刺激的心血管功能的影响。方法和结果:?从怀孕的第6天到第20天,对Wistar大鼠进行常氧,低氧(13%O 2 ),低氧+维生素C(饮用水中5mg / ml)或常氧+维生素C。在第4个月时,对雄性后代进行尿烷麻醉。评估基础平均动脉血压,心率和心率变异性(HRV),并用去氧肾上腺素和硝普钠生成刺激的压力反射曲线。慢性胎儿缺氧会增加LF / HF HRV比和压力反射增加,在怀孕期间服用维生素C可以防止这种影响。结论:?慢性宫内缺氧可引起成年大鼠后代体内心血管功能障碍。数据支持通过母体维生素C改善这种作用。该数据通过在子宫内产生氧化应激,支持胎儿慢性低氧在体内对成年大鼠后代的心血管功能障碍进行编程。(Circ J?2013; 77:2604–2611 )

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