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人们在吸入含有二氧化硫(SO2)的空气会出现鼻阻塞反应。本研究使用麻醉猪测量SO2对鼻腔血管和气道阻力的影响以及其控制机制。将相同通气量的空气从呼出方向通入两侧鼻腔或直接经支气管入肺,测量鼻腔及支气管的气流压力并计算鼻腔及支气管气流阻力的改变。同时记录体动脉的压力和鼻腔动脉的血流量以计算血管阻力的变化。空气中含有2 ppm SO2时,血压及鼻血管阻力下降但鼻气道及支气管阻力上升。空气中SO2含量上升至8 ppm时,血压、鼻血管阻力和支气管气流阻力均上升,但鼻气道阻力下降。直接鼻腔刺激和经支气管入肺引起的反应相同。单侧鼻腔刺激引出双侧反应。钌红抑制鼻腔刺激反应。两侧迷走交感神经切除抑制肺刺激反应。因此2 ppm SO2引起经受体反射鼻血管扩张令鼻阻塞,而较高浓度SO2引发经受体反射鼻血管收缩令鼻阻塞减轻。短时间暴露(STEL)于2 ppm SO2所引起鼻阻塞及支气管收缩可限制SO2进入肺部,而较高浓度SO2引发鼻阻塞减轻可令总气道阻力下降以对抗支气管收缩产生的肺通气减少。
Nasal obstruction occurs when inhaling air containing sulfur dioxide (SO2). This study used anesthetized pigs to measure the effects of SO2 on nasal vascular and airway resistance and their mechanisms of control. The same amount of ventilation air from the direction of exhalation into both sides of the nasal cavity or directly through the bronchial lungs, nasal and bronchial air flow pressure measurement and calculation of nasal and bronchial airflow resistance changes. At the same time, the pressure of the artery and the blood flow of the nasal artery were recorded to calculate the change of the vascular resistance. When air contains 2 ppm SO2, blood pressure and nasal vascular resistance decrease but nasal airway and bronchial resistance rise. As the SO2 concentration in the air rose to 8 ppm, blood pressure, nasal vascular resistance and bronchial airflow resistance increased, but nasal airway resistance decreased. Direct nasal stimulation and bronchial lungs caused the same response. Unilateral nasal stimulation leads to bilateral reactions. Ruthenium red suppresses nasal irritation. Vaginal sympathectomy on both sides suppresses pulmonary stimulation. Thus 2 ppm SO2 causes nasal obstruction by receptor-reflecting nasal dilatation, whereas higher concentrations of SO2 cause nasal obstruction to be attenuated by receptor contractile nasal vasoconstriction. Nasal and bronchoconstriction induced by STEL at 2 ppm SO2 limits the entry of SO2 into the lungs, whereas reduction of the nasal obstruction with higher concentrations of SO2 causes a decrease in total airway resistance to counteract the reduction of lung ventilation due to bronchoconstriction.