Brown R H, Herold C, Zerhouni E A, Mitzner W
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore.
Chest. 1994 Sep;106(3):920-4. doi: 10.1378/chest.106.3.920.
Airway constriction during a breath hold could not be examined previously using standard methods. We used high-resolution computed tomography (HRCT) in vivo to assess the temporal changes in airway area and the effects of a deep inspiration with and without vagal suppression. Five dogs were anesthetized, intubated, and their lungs ventilated with 100 percent oxygen. Fifteen HRCT slices were obtained at functional residual capacity (FRC) either immediately after stopping ventilation at end expiration after either a tidal volume breath or three deep inspirations. Subsequently the dogs were given atropine, 0.2 mg/kg, and the scans were repeated. The cross-sectional areas of 33 airways ranging in size from 1.6 to 9.7 mm in diameter were measured. Airways were separated in three groups based on size: small (< 3 mm in diameter); medium (3 to 6-mm in diameter); and large (> 6 mm in diameter). The small, medium, and large airways showed a spontaneous constriction over time to 49 +/- 8 percent, 83 +/- 4 percent, and 82 +/- 4 percent of initial airway size, respectively (p < 0.01), (p < 0.0001). The deep inspiration caused an initial dilation only in the smallest airways to 133.3 +/- 4 percent. The subsequent constrictions were even greater than after the tidal volume breath averaging 67 +/- 15 percent, 61 +/- 6 percent, and 60 +/- 9 percent of initial airway area in the small, medium, and large airways, respectively (p = 0.001). Atropine caused an average increase in baseline airway area of 115 +/- 5 percent and 121 +/- 6 percent after a tidal volume breath and deep inspiration, respectively, compared with the preatropine controls, with no difference between the three groups. Atropine also completely abolished the spontaneous airway constriction observed after either a tidal volume breath or a deep inspiration in all three groups equally. In conclusion, using direct airway imaging in vivo, we found that airways spontaneously constrict during a prolonged expiratory pause, and a deep inspiration significantly augments this airway constriction. These responses are mediated via vagal afferent pathways, likely arising from progressively decreasing slow-adapting receptor activity.
以往使用标准方法无法检查屏气期间的气道收缩情况。我们在体使用高分辨率计算机断层扫描（HRCT）来评估气道面积的时间变化以及深吸气（有无迷走神经抑制）的影响。五只狗麻醉后插管，并用100%氧气进行肺通气。在潮气量呼吸或三次深吸气后呼气末停止通气后，立即在功能残气量（FRC）下获取15层HRCT切片。随后给狗注射0.2mg/kg阿托品，并重复扫描。测量了33条直径从1.6到9.7mm的气道的横截面积。气道根据大小分为三组：小气道（直径<3mm）；中等气道（直径3至6mm）；大气道（直径>6mm）。小气道、中等气道和大气道随时间自发收缩至初始气道大小的49±8%、83±4%和82±4%，分别（p<0.01），（p<0.0001）。深吸气仅使最小气道初始扩张至133.3±4%。随后的收缩甚至大于潮气量呼吸后的收缩，小气道、中等气道和大气道分别平均为初始气道面积的67±15%、61±6%和60±9%（p = 0.001）。与阿托品给药前的对照组相比，阿托品分别使潮气量呼吸和深吸气后的基线气道面积平均增加115±5%和121±6%，三组之间无差异。阿托品还同样完全消除了三组在潮气量呼吸或深吸气后观察到的气道自发收缩。总之，通过在体直接气道成像，我们发现气道在延长的呼气暂停期间自发收缩，深吸气显著增强这种气道收缩。这些反应是通过迷走神经传入途径介导的，可能源于逐渐降低的慢适应性受体活性。
