Sasaki K, Nadel J A, Hahn H L
J Appl Physiol (1985). 1987 Jan;62(1):15-26. doi: 10.1152/jappl.1987.62.1.15.
We exposed two awake dogs with a chronic tracheostomy and the cervical vagus nerves exteriorized in skin loops to 1.0 ppm of ozone (O3) for 2 h at intervals of 4 wk. We measured ventilatory variables before and after O3 exposure during rest and exercise before and after vagal block. We compared the effects of vagal blockade, exercise, and O3 on the primary determinants of breathing pattern (VT/TI, VT/TE, TI, and TE) in each of three conditions: base line (steady state), during hypercapnia, and after inhalation of 1% histamine. Under base-line conditions, O3 increased respiratory rate and decreased tidal volume (VT) by shortening time of expiration (TE) and time of inspiration (TI) without affecting VT/TI, an indicator of the neural drive to breathing. During progressive hypercapnia, O3 shortened TE and TI by effects both on tonic (nonvolume-related) and on phasic (volume-related) vagal inputs, and only the latter were prevented completely by cooling of the vagus nerves. Histamine-induced tachypnea was increased by O3 and was totally blocked by cooling the vagus nerves. We conclude that O3 shortens the timing of respiration without increasing ventilatory drive, shortens TI and TE through vagal and nonvagal pathways, increases tonic nonvagal and phasic vagal inputs, and stimulates more than one vagal fiber type.
我们将两只患有慢性气管造口术且颈迷走神经游离于皮肤环中的清醒犬，每隔4周暴露于1.0 ppm的臭氧（O₃）中2小时。我们在迷走神经阻断前后的静息和运动期间，测量了臭氧暴露前后的通气变量。我们比较了迷走神经阻断、运动和臭氧对三种情况下呼吸模式主要决定因素（潮气量/吸气时间、潮气量/呼气时间、吸气时间和呼气时间）的影响：基线（稳态）、高碳酸血症期间以及吸入1%组胺后。在基线条件下，臭氧通过缩短呼气时间（TE）和吸气时间（TI）增加呼吸频率并降低潮气量（VT），而不影响作为呼吸神经驱动指标的潮气量/吸气时间。在进行性高碳酸血症期间，臭氧通过对紧张性（与容积无关）和相位性（与容积有关）迷走神经输入的作用缩短TE和TI，并且只有后者通过冷却迷走神经被完全阻断。臭氧增加了组胺诱导的呼吸急促，并且通过冷却迷走神经被完全阻断。我们得出结论，臭氧缩短呼吸时间而不增加通气驱动，通过迷走神经和非迷走神经途径缩短TI和TE，增加紧张性非迷走神经和相位性迷走神经输入，并刺激不止一种迷走神经纤维类型。
