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Acute inhalation of ozone induces vagally mediated rapid shallow breathing and bronchoconstriction. In spontaneously breathing anesthetized dogs, we attempted to determine whether afferent vagal C-fibers in the lower airways contributed to these responses. Dogs inhaled 3 ppm ozone for 40-70 min into the lower trachea while cervical vagal temperature was maintained successively at 37, 7, and 0 degrees C. At 37 degrees C, addition of ozone to the inspired air decreased tidal volume and dynamic lung compliance and increased breathing frequency, total lung resistance, and tracheal smooth muscle tension. Ozone still evoked significant effects when conduction in myelinated vagal axons was blocked selectively by cooling the nerves to 7 degrees C. Ozone-induced effects were largely abolished when nonmyelinated vagal axons were blocked by cooling to 0 degree C, breathing during ozone inhalation at 0 degree C being generally similar to that during air breathing at 0 degree C, except that minute volume and inspiratory flow were higher. We conclude that afferent vagal C-fibers in the lower airways make a major contribution to the acute respiratory effects of ozone and that nonvagal afferents contribute to the effects that survive vagal blockade.

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We examined the contribution of afferent vagal A- and C-fibers on abdominal expiratory muscle activity (EMA). In seven spontaneously breathing supine dogs anesthetized with alpha-chloralose we recorded the electromyogram of the external oblique muscle at various vagal temperatures before and after the induction of a pneumothorax. When myelinated fibers were blocked selectively by cooling the vagus nerves to 7 degrees C, EMA decreased to 40% of control (EMA at 39 degrees C). With further cooling to 0 degrees C, removing afferent vagal C-fiber activity, EMA returned to 72% of control. On rewarming the vagus nerves to 39 degrees C, we then induced a pneumothorax (27 ml/kg) that eliminated the EMA in all the dogs studied. Cooling the vagus nerves to 7 degrees C, during the pneumothorax, produced a slight though not significant increase in EMA. However, further cooling of the vagus nerves to 0 degrees C caused the EMA to return vigorously to 116% of control. In three dogs, intravenous infusion of a constant incrementally increasing dose of capsaicin, a C-fiber stimulant, decreased EMA in proportion to the dose delivered. These results suggest that EMA is modulated by a balance between excitatory vagal A-fiber activity, most likely from slowly adapting pulmonary stretch receptors, and inhibitory C-fiber activity, most likely from lung C-fibers.

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Objective:To compare the efficacy of percutaneous transtracheal ventilation (PTV) in the unparalyzed state with that in the paralyzed state using a sedated nonobstructed canine model. Methods: Eight mongrel dogs (16.8-32 kg) were anesthetized, instrumented, and placed in a volume plethysmograph. Anesthesia was achieved with pentobarbital sodium (up to 30 mgkg). The spontaneous respiratory drive was kept intact. PTV was performed using a 13-ga transtracheal catheter and compressed air at 45 psi at an I:E ratio of 1:3 (15 breathdmin). Each dog was sequentially ventilated in both the paralyzed and unparalyzed states. The paralyzedunparalyzed sequence was alternated among the animals to avoid sequence bias. Paralysis was achieved with succinylcholine (0.1 mgkg bolus and 0.01 mg/kg/min drip). Reversal of paralysis was achieved by discontinuing the succinylcholine infusion. Key variables, including arterial blood gas, tidal volume, and pulmonary mechanics, were measured and compared for the paralyzed and unparalyzed states. Results: Gas exchanges and lung mechanics were similar between the unparalyzed and paralyzed states. There was no significant difference in mean pH, pC02, pO2. tidal volume, or peak inspiratory transpulmonary pressure. There was also no significant difference in pulmonary resistance or pulmonary compliance. Conclusion: In a sedated nonobstructed canine model, PTV is as efficacious in the unparalyzed state as it is in the paralyzed state. The lung mechanics are also similar in the 2 states. These data suggest that it may be unnecessary to induce paralysis when using PTV for emergency ventilation in the heavily sedated state.