PROTECTIVE VENTILATORY RESPONSES TO HYPOXIA

对缺氧的保护性反应分为两层。与 初始暴露，正常呼吸通气量增加。严重缺氧时， 取而代之的是喘息，这促进了“自动复苏”。" 正常人对缺氧的呼吸反应随发育而变化。在 新生儿的通气量上升然后福尔斯下降。随着年龄的增长缺氧 诱导扩增变得更加持久。我们假设缺氧- 诱发性抑郁症是由中脑- 脑桥“中央氧气探测器。" 将对仔猪进行研究。我们将确定包含 “中央氧气探测器。“缺氧引起的通气抑制 如果这个中央氧的神经元被破坏，神经元 将对该探测器的活动进行表征。这些活动 假设在膈神经活动抑制期间增加， 缺氧或在局部缺氧期间通过应用氰化钠。 然后，我们将研究腹侧延髓神经元在 缺氧诱导的代偿性抑郁症和神经发生 喘着气这些腹侧延髓神经元活动可能提供了一个 一般性紧张性输入，用于解释性活动。但喘息不会是 改变，因为神经发生的基础机制， 喘息有本质上的不同。 在未麻醉的仔猪中，将在麻醉期间记录排泄活动。 清醒和睡眠。我们假设呼吸暂停发作 在延髓喘息中心的神经元消融后记录， 位于腹侧髓质的 我们的研究结果将对呼吸暂停的机制产生深远的影响 和婴儿猝死综合症中枢性呼吸暂停的机制可能是 我们的研究阐明了缺氧对大脑的“直接”影响， 脑干腹侧延髓的作用 机制，在这种缺氧诱导的抑郁症和延髓的作用， 控制正常呼吸的喘息机制。

The protective response to hypoxia is organized in two layers. With initial exposure, eupneic ventilation increase. In severe hypoxia, eupnea is replaced by gasping, which promotes "autoresuscitation." The eupneic ventilatory response to hypoxia changes with development. In the newborn, ventilation rises and then falls. With age, the hypoxia- induced augmentation becomes more sustained. We hypothesize that hypoxia- induced ventilatory depression results from activation of a mesencephalic- pontine "central oxygen detector." Piglets will be studied. We will identify the region containing the "central oxygen detector." Hypoxia-induced depressions of ventilation will be attenuated if neurons of this central oxygen are destroyed. Neuronal activities of this detector will be characterized. These activities are hypothesized to increased during depressions of phrenic activity in hypoxia or during localized hypoxia by applications of sodium cyanide. We will then examine the role of neurons in the ventral medulla in hypoxia-induced ventilatory depressions and in the neurogenesis of gasping. These ventral medullary neuronal activities may provide a generalized tonic input for ventilatory activity. Yet gasping will not be altered since the mechanisms underlying the neurogenesis of eupnea and gasping differ fundamentally. In unanesthetized piglets, ventilatory activity will be recorded during wakefulness and sleep. We hypothesize that apneic episodes will be recorded following ablation of neurons in the medullary gasping center and those in the ventral medulla. Our results will have profound implications as to the mechanisms of apnea and the sudden infant death syndrome. Mechanisms of central apnea may be elucidated by our studies of the "direct" influence of hypoxia on the brainstem ventilatory control system, of the role of ventral medullary mechanisms in this hypoxia-induced depression and the role of medullary gasping mechanisms in the control of eupnea.