首页> 外文期刊>The Journal of Physiology >Long-term facilitation of ventilation following repeated hypoxic episodes in awake goats.
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Long-term facilitation of ventilation following repeated hypoxic episodes in awake goats.

机译:在清醒的山羊中反复缺氧发作后,长期促进通气。

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1. This study tested two hypotheses: (1) that episodic hypoxia elicits long-term facilitation (LTF) in respiratory neurons that is manifest as an increase in ventilation in awake goats; and (2) that LTF causes complex changes in respiratory pattern which are responsible for the increase in ventilation. 2. Each goat participated in two protocols. In the first, inspired gas mixtures were alternated between isocapnic normoxia and hypoxia (arterial partial pressure of oxygen, Pa,O2 = 47 mmHg) for ten cycles. Each hypoxic episode lasted 3 min and normoxic intervals were 5 min. Ventilatory variables were measured during the last minute of each episode and periodically for up to 1 h following the last hypoxic episode. The second, sham protocol was undertaken at least 2 weeks later and was identical to the first, except that isocapnic hypoxia was replaced with normoxia. 3. Inspired ventilation (VI) increased during the first isocapnic hypoxic episode and reached progressively higher levels in subsequent hypoxic episodes. VI also increased progressively among normoxic intervals, such that by the tenth normoxic interval, it had increased 68% relative to the comparable sham value (P < 0.05). Respiratory frequency (FR), tidal volume and mean inspiratory flow all contributed to the augmented VI during both isocapnic normoxia and hypoxia. The increase in VI lasted up to 40 min after the final hypoxic episode, with an increased FR making the greatest contribution. The persistent increase in VI strongly suggests that episodic hypoxia elicits LTF in respiratory neurons in the awake goat. Complex changes in respiratory pattern underpin the ventilatory manifestation of LTF.
机译:1.这项研究检验了两个假设:(1)突发性缺氧会引起呼吸神经元的长期促进(LTF),这表现为清醒山羊的通气增加; (2)LTF会导致呼吸模式的复杂变化,从而导致通气量增加。 2.每只山羊都参加了两个协议。首先,将吸入的混合气体在等高碳酸血症和缺氧(氧气的动脉分压,Pa,O2 = 47 mmHg)之间交替进行十个循环。每次缺氧持续3分钟,常氧间隔为5分钟。在每个发作的最后一分钟测量通气量,并在最后一次缺氧发作后的1h内定期测量通气量。第二次假手术至少在两周后进行,与第一个相同,只是用等氧代替了低碳酸血症。 3.吸入性通气(VI)在第一个等碳酸血症低氧发作期间增加,并在随后的低氧发作中逐渐升高。 VI在常氧间隔之间也逐渐增加,因此到第十个常氧间隔,相对于可比较的假手术值,VI增加了68%(P <0.05)。在等碳酸血症常氧和低氧期间,呼吸频率(FR),潮气量和平均吸气流量均导致VI增加。最终的低氧发作后,VI的持续时间长达40分钟,FR的增加是最大的贡献。 VI的持续增加强烈表明,发作性缺氧会在清醒的山羊呼吸神经元中引发LTF。呼吸模式的复杂变化是LTF通气表现的基础。

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