MECHANISMS AND SITES OF VENTILATORY NEUROGENESIS

描述（改编自申请人摘要）：“自动”呼吸 没有意识的运动，是在大脑内部产生的。 脑干的脑桥和髓质部分。有几种模式 “自动”通风。Eupnea是“正常”呼吸。在正常呼吸中， 氧气被供应给身体，二氧化碳被排出，以满足新陈代谢的需要。 要求。如果正常呼吸停止，就会出现缺氧。严重缺氧新兵 喘息，这是一种强大的防御机制， “自动复苏”“一个基本问题涉及具体的 产生正常呼吸和喘息的神经生理机制。严重 缺氧时，假设延髓的潜在起搏放电 呼吸神经元被释放以产生喘息。在呼吸正常的情况下， 活动被纳入脑桥延髓神经元回路负责 正常呼吸的神经发生。神经生理学的定义 负责这一合并的过程将增强我们对以下方面的理解： 正常呼吸的神经发生这些研究要求可逆的 正常呼吸改变为喘息。此外，为了评估 各种假定的神经递质在神经发生，药理学 药剂将被全身施用，以及通过 微离子导入法灌注的“幼年大鼠”是唯一适合于 这些研究的成功。由于系统性“呼吸”和 这种制剂的“循环”系统被体外“替代”， 在缺氧诱导的循环中，没有心力衰竭的可能性 喘着气同样，可以施用药理学试剂，其将 几乎肯定会损害心血管功能和体内 准备.这些研究的结果将提供重要的信息， 产生正常呼吸的机制。这样的信息可以 提供了对人体通气控制功能障碍的深入了解， 如“睡眠呼吸暂停”或“婴儿猝死综合征”。"

DESCRIPTION (Adapted from the applicant's abstract):"Automatic" breathing movements, which occur without conscious effort, are generated within the pontile and medullary portions of the brainstem. There are several patterns of "automatic" ventilation. Eupnea is "normal" breathing. In eupnea, sufficient oxygen is supplied to the body and carbon dioxide removed to meet metabolic demands. If eupnea ceases, hypoxia will develop. Severe hypoxia recruits gasping, which serves as a powerful defensive mechanism for "autoresuscitation." A fundamental question concerns the specific neurophysiological mechanisms which generate eupnea and gasping. In severe hypoxia, it is hypothesized that a latent pacemaker discharge of medullary respiratory neurons is released to generate the gasp. In eupnea, this pacemaker activity is incorporated into the pontomedullary neuronal circuits responsible for the neurogenesis of eupnea. A definition of the neurophysiological processes responsible for this incorporation will enhance our understanding of the neurogenesis of eupnea, per se. The studies proposed require the reversible alteration of eupnea to gasping. Moreover, in order to evaluate the role of various putative neurotransmitters in ventilatory neurogenesis, pharmacological agents will be administered systemically, as well as onto neurons by microiontophoresis. The perfused "juvenile rat" is uniquely suited for the successful performance of these studies. Since the systemic "respiratory" and "circulatory" systems of this preparation are "replaced" by an extracorporeal circuit, there is no possibility of cardiac failure during hypoxia-induced gasping. Likewise, pharmacological agents can be administered which would almost certainly compromise cardiovascular function and viability of an in vivo preparation. Results of these studies will provide significant information into the mechanisms by which normal breathing is generated. Such information might provide insights into dysfunctions of the control of ventilation in humans, such as in "sleep apneas" or the "sudden infant death syndrome."