McCaffrey T V, Kern E B
Acta Otolaryngol. 1979 May-Jun;87(5-6):545-53. doi: 10.3109/00016487909126463.
Nasal airway resistance was calculated in 9 anesthetized mongrel dogs by measuring the pressure difference across the nasal airway while a continuous flow of humidified air was passed through the upper airway. Hypercapnia produced a significant decrease in nasal airway resistance (P less than 0.05, Wilcoxon signed-rank test), which was proportional to the Paco2 over the range of 40 to 70 torr. Hypoxia produced a decrease in nasal airway resistance only when there was severe depression of Pao2. Direct stimulation of peripheral chemoreceptors by intravenously administered NaCN (100 microgram/kg) resulted in a significant decrease in nasal airway resistance (P = 0.06, Wilcoxon signed-rank test). Interruption of the cervical sympathetic trunk bilaterally abolished or reversed the response of the nasal airway resistance to hypercapnia and to NaCN. The study indicates that the nasal airway can modify airway resistance in response to respiratory stimuli and that this reflex is mediated by the sympathetic nervous system.
在9只麻醉的杂种犬中,通过测量当加湿空气持续流经上呼吸道时鼻气道两端的压力差来计算鼻气道阻力。高碳酸血症导致鼻气道阻力显著降低(P<0.05,Wilcoxon符号秩检验),在40至70托的范围内,该降低与动脉血二氧化碳分压(Paco2)成比例。低氧仅在动脉血氧分压(Pao2)严重降低时才导致鼻气道阻力降低。静脉注射氰化钠(100微克/千克)直接刺激外周化学感受器导致鼻气道阻力显著降低(P = 0.06,Wilcoxon符号秩检验)。双侧切断颈交感干消除或逆转了鼻气道阻力对高碳酸血症和氰化钠的反应。该研究表明,鼻气道可响应呼吸刺激而改变气道阻力,且该反射由交感神经系统介导。