首页> 外文期刊>The Journal of Physiology >Lack of involvement of the autonomic nervous system in early ventilatory and pulmonary vascular acclimatization to hypoxia in humans.
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Lack of involvement of the autonomic nervous system in early ventilatory and pulmonary vascular acclimatization to hypoxia in humans.

机译:自主神经系统缺乏参与早期通气和肺血管适应低氧的能力。

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The activity within the autonomic nervous system may be altered following sustained exposure to hypoxia, and it is possible that this increase in activity underlies the early acclimatization of both ventilation and the pulmonary vasculature to hypoxia. To test this hypothesis, seven individuals were infused with the ganglionic blocker trimetaphan before and after an 8 h exposure to hypoxia. The short half-life of trimetaphan should ensure that the initial infusion does not affect acclimatization to the 8 h hypoxia exposure, and the use of a ganglion blocking agent should inhibit activity within all branches of the autonomic nervous system. During the infusions of trimetaphan, measurements of ventilation and echocardiographic assessments of pulmonary vascular tone (DeltaPmax) were made during euoxia and during a short period of isocapnic hypoxia. Subjects were also studied on two control days, when a saline infusion was substituted for trimetaphan. Trimetaphan had no effect on either euoxic ventilation or the sensitivity of ventilation to acute hypoxia. Trimetaphan significantly reduced DeltaPmax in euoxia (P<0.05), but had no significant effect on the sensitivity of DeltaPmax to acute hypoxia once changes in cardiac output had been controlled for. The 8 h period of hypoxia elevated euoxic ventilation (P<0.001) and DeltaPmax (P<0.001) and increased their sensitivities to acute hypoxia (P<0.001 for both), indicating that significant acclimatization had occurred. Trimetaphan had no effect on the acclimatization response of any of these variables. We conclude that altered autonomic activity following 8 h of hypoxia does not underlie the acclimatization observed in ventilation or pulmonary vascular tone.
机译:持续暴露于缺氧状态下,自主神经系统内的活动可能会发生改变,这种活动的增加可能是通气和肺血管系统早期适应缺氧的基础。为了检验该假设,在缺氧8小时之前和之后,向7名个体注入了神经节阻滞剂曲美他汀。曲美他芬的半衰期短,应确保初始输注不会影响8 h低氧暴露的适应,并且使用神经节阻滞剂应抑制植物神经系统所有分支的活动。在输注曲美他全期间,在充血和短时等碳酸血症性缺氧期间进行通气测量和超声心动图评估肺血管张力(DeltaPmax)。还用盐水注入代替曲美他汀的两个对照日对受试者进行了研究。 Trimetaphan对常压通气或通气对急性缺氧的敏感性均无影响。 Trimetaphan可以显着降低欧洲人的DeltaPmax(P <0.05),但是一旦控制了心输出量的变化,对DeltaPmax对急性缺氧的敏感性没有明显影响。缺氧的8小时时段内,高氧通气(P <0.001)和DeltaPmax(P <0.001)升高,并且它们对急性缺氧的敏感性增加(两者均P <0.001),表明发生了显着的适应性。 Trimetaphan对这些变量中任何一个的驯化响应均没有影响。我们得出的结论是,缺氧8小时后自主神经活动的改变并不构成通气或肺血管紧张状态中观察到的适应能力的基础。

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