Effect of changes in blood gas tensions and carotid sinus pressure on tracheal volume and total lung resistance to airflow
Effect of changes in blood gas tensions and carotid sinus pressure on tracheal volume and total lung resistance to airflow
复制标题
血气张力和颈动脉窦压力变化对气管容量和肺气流总阻力的影响
DOI：
--
复制
发表时间：
1962
期刊：
影响因子：
--
通讯作者：
J. G. WIDDICOMBEt
中科院分区：
文献类型：
--
作者：
BY J. A. Nadel;J. G. WIDDICOMBEt
窒息、高碳酸血症和低氧血症使气管(Loofbourrow，Wood&Baird，1957)和支气管(Roy&Brown，1885)收缩，也改变了肺的机械性能，可归因于支气管收缩(Einthven，1892；Dixon&Brodie，1903)。这些效应在很大程度上依赖于迷走神经传导的完整性。在分析相关机制时，Daly&Schweitzer(1951)得出结论，刺激狗的颈动脉小体化学感受器会引起反射性支气管扩张，Daly，Lambertsen&Schweitzer(1953)认为中枢神经系统的低氧血症和高碳酸血症产生神经性介导的支气管收缩。上面引用的实验通常涉及在潮气量周期性变化期间评估通胀压力和潮气量之间的关系。与电学理论类似，这种关系与呼吸系统的“阻抗”密切相关。在本文中，将使用术语阻抗来描述这些测量。在通常的换气频率下，阻抗测量对气道阻力的变化非常不敏感，并且受到顺应性变化的很大影响。因此，基于阻抗测量的结果不能明确地归因于气道阻力的变化，也不能给出关于气道直径的定量信息。本文描述了低氧血症、高碳酸血症和颈动脉窦压力变化对犬气管段容量和总肺阻力的作用。我们还研究了调节这些变化的神经机制，控制了通气率和深度，并试图消除肺顺应性和跨肺压变化的影响。一些结果的摘要已经出版(Nadel&Widdicombe，1961)。
Asphyxia, hypercapnia and hypoxaemia constrict the trachea (Loofbourrow, Wood & Baird, 1957) and bronchi (Roy & Brown, 1885), and also change the mechanical properties of the lungs in a manner attributed to bronchoconstriction (Einthoven, 1892; Dixon & Brodie, 1903). These effects are largely dependent on the integrity of vagal conduction. In analysing the responsible mechanisms Daly & Schweitzer (1951) concluded that stimulation of carotid body chemoreceptors in dogs causes reflex bronchodilatation, and Daly, Lambertsen & Schweitzer (1953) decided that hypoxaemia and hypercapnia of the central nervous system produce nervously mediated bronchoconstriction. The experiments cited above usually involved assessment ofthe relationship between inflation pressure and tidal volume during cyclical changes in volume. This relationship is, by analogy to electrical theory, closely related to the 'impedance' of the respiratory system. The term impedance will be used to describe these measurements in this paper. At the usual frequencies of ventilation, impedance measurements are very insensitive to changes in airway resistance and greatly influenced by alterations in compliance. Therefore, results based on impedance measurements cannot be unequivocally attributed to changes in airway resistance, and give no quantitative information about airway diameter. This paper describes the actions of hypoxaemia, hypercapnia, and changes in carotid sinus pressure on the volume of a tracheal segment and on the total lung resistance to airflow in dogs. We have also studied the nervous mechanisms mediating these changes and have controlled the rate and depth of ventilation and attempted to eliminate the effects of changes in lung compliance and transpulmonary pressure. An abstract of some of the results has been published (Nadel & Widdicombe, 1961).