PROTECTIVE VENTILATORY RESPONSES TO HYPOXIA

对低氧的保护反应由两层组成。使用 初次暴露时，常压通气量增加。在严重缺氧时，真呼吸暂停 取而代之的是喘息，这促进了“自动复苏”。 对低氧的呼吸反应会随着发育而改变。在……里面 新生儿，通气量上升，然后下降。随着年龄的增长，缺氧- 诱导增强变得更加持久。我们假设缺氧- 诱导的呼吸性抑制是由于激活了中脑- 庞蒂市的“中央氧气探测器”。 将对仔猪进行研究。我们将标识包含 “中央氧气探测器。”低氧所致的通气量下降 如果这种中枢氧气的神经元被破坏，就会减弱。神经元 将对该探测器的活动进行表征。这些活动是 假设在膈神经活动抑制期间增加 低氧或局部低氧时使用氰化钠。 然后我们将研究腹侧延髓中神经元在 低氧所致的呼吸性抑郁及其在神经发生中的作用 气喘吁吁。这些延髓腹侧神经元的活动可能为 用于换气活动的通用补药输入。然而，喘息不会 改变了自发性呼吸暂停和呼吸暂停的神经发生机制 喘息从根本上说是不同的。 在未麻醉的仔猪中，呼吸活动将在 清醒和睡眠。我们假设呼吸暂停发作将是 消融延髓喘息中心神经元后的记录 在延髓腹侧的那些。 我们的结果将对呼吸暂停的机制产生深远的影响。 以及婴儿猝死综合症。中枢性呼吸暂停的机制可能是 通过我们对低氧对细胞的“直接”影响的研究来阐明 脑干通风控制系统对延髓腹侧的作用 缺氧性抑郁的机制及延髓的作用 呼吸困难控制中的喘息机制。

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.