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Reactive oxygen species from NADPH oxidase contribute to altered pulmonary vascular responses in piglets with chronic hypoxia-induced pulmonary hypertension

机译:来自NADPH氧化酶的反应性氧气含有慢性缺氧诱导的肺动脉高压的仔猪肺血管反应有助于改变肺血管反应

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Regulation of pulmonary vascular tone is also known to differ between large, conduit level arteries and smaller, resistance level arteries (1, 2, 45). The vast majority of studies to date have evaluated the potential contribution from ROS to abnormal reactivity in larger, conduit level vessels (20, 37, 38, 53). Because of their critical role in regulating pulmonary vascular tone, it is important to identify derangements in ROS in resistance level pulmonary arteries. We previously showed that resistance level pulmonary arterial responses to acetylcho-line (ACh) are altered in newborn piglets with pulmonary hypertension induced by 3 days' exposure to hypoxia (17-19). The major purpose of this study was to test the hypothesis that ROS are involved with the aberrant responses to ACh that develop in resistance pulmonary arteries (PRAs) at this early stage of pulmonary hypertension in newborn piglets. In addition, we wanted to determine whether NADPH oxidase is an enzymatic source of ROS in the PRAs of piglets with chronic hypoxia-induced pulmonary hypertension
机译:肺血管间调的调节也已知在大,导管水平动脉和较小的抗性水平动脉(1,2,45)之间不同。迄今为止的绝大多数研究已经评估了ROS在较大的导管水平容器(20,37,38,53)中对异常反应性的潜在贡献。由于它们在调节肺血管基调方面的关键作用,因此重要的是鉴定抗性水平肺动脉的ROS中的紊乱。我们以前表明,对乙酰糠醛(ACH)的阻力水平肺动脉应答在新生仔猪中改变,肺动脉高血压诱导3天暴露于缺氧(17-19)。本研究的主要目的是测试ROS参与对新出生仔猪肺动脉高压肺动脉肺动脉(PRA)在抗性肺动脉(PRA)的异常反应的假设。此外,我们想确定NADPH氧化酶是否是猪缺氧诱导的肺动脉高压仔猪中的ROS的酶源

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