PERIPHERAL AND CENTRAL VENTILATORY CONTROL

我们的主要目标是加强对通风控制的了解。 系统。我们的具体目标是增加对两国关系的了解 颈动脉小体(CB)化学感受器与中枢呼吸控制 机械装置。我们将研究呼吸习服的机制 慢性缺氧(VACH)，CB中O2和CO2之间的相互作用，以及 不同的脑氧合对CB化学感受器输入的影响。 将使用两种实验方法：a)将CB灌注到 使用新开发的分离和控制方法唤醒山羊 动脉血气到达脑脊液和大脑。B)补充 上述灌流研究为心脏功能增加了新的认识。 CB，我们将对CB传入活动进行长期(小时)记录 麻醉的山羊。 在CB灌流模型中，供应一侧大脑的血管是 结扎，但从对侧供应的脑血流 血管保持正常。在结扎部位插入血管分流管 颈动脉，允许CB，但不允许脑灌流，通过 体外循环。另一个CB将被移除。我们已经找到了 通常对CB刺激有反应的准备，并已完成 使用模型的研究表明，在不存在Vach的情况下可以发生Vach 脑部缺氧。 我们将检查的问题是：a)脑碱中毒是 瓦奇？B)非缺氧性CB刺激(高碳酸血症)是否会导致 适应？C)CB传入活动是否发生随时间变化 超过几个小时的低氧或高二氧化碳的CB刺激？D)是CB多巴胺 参与VACH的受体？E)CB中O2和CO2的相互作用是什么 它们与清醒的山羊的呼吸有关联吗？F)如何 脑内氧气水平影响对CB的呼吸反应 刺激？ 这些研究为解决一些长期悬而未决的问题提供了一种新的方法 将有助于我们了解大脑和CB的不同角色 在通风控制方面。所获得的数据将加深我们对 以慢性缺氧和/或疾病为特征的病理生理学 高碳酸血症。

Our major objective is to enhance understanding of the ventilatory control system. Our specific goal is to increase knowledge of the relationship between carotid body (CB) chemoreceptor and CNS ventilatory control mechanisms. We will examine mechanisms of ventilatory acclimatization to chronic hypoxia (VACH), interactions between O2 and CO2 in the CB, and the effects of varying cerebral oxygenation on input from CB chemoreceptors. Two experimental approaches will be used: a) perfusion of the CB in the awake goat using newly developed methods that allow separation and control of arterial blood gases reaching the CB and the brain. b) To complement the above perfusion studies and add new knowledge to the function of the CB, we will do long term (hours) recording of CB afferent activity in anesthetized goats. In the CB perfusion model, vessels supplying one side of the brain are ligated but the brain blood flow which is supplied from the contralateral vessels remains normal. A vascular shunt is inserted in the ligated site carotid artery which allows perfusion of the CB, but not the brain, by an extracorporeal circuit. The other CB is removed. We have found the preparation normally responsive to CB stimulation and have completed a study using the model demonstrating that VACH can occur in the absence of brain hypoxia. The questions we will examine are: a) Is cerebral alkalosis a component of VACH? b) Does non-hypoxic CB stimulation (hypercapnia) induce acclimatization? c) Do time-dependent changes in CB afferent activity occur over hours of hypoxic or hypercapnic CB stimulation? d) Are CB dopamine receptors involved in VACH? e) What are O2 and CO2 interactions at the CB and do they correlate with ventilation in the awake goat? f) How does the level of O2 in the brain influence the ventilatory response to CB stimulation? These studies provide a new approach to some long unanswered questions and will contribute to our knowledge of the separate roles of the brain and CB in ventilatory control. The data obtained will add to our understanding of the pathophysiology of diseases characterized by chronic hypoxia and/or hypercapnia.