Chronic passive cigarette smoke exposure augments bronchopulmonary C‐fibre inputs to nucleus tractus solitarii neurones and reflex output in young guinea‐pigs

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Abstract
Children chronically exposed to environmental tobacco smoke (passive cigarette smoke) have more wheeze, cough, bronchoconstriction, airway hyper‐reactivity and mucous secretion, which may result, in part, from stimulation of the vagal bronchopulmonary C‐fibre reflex. Environmental tobacco smoke increases the sensitivity of bronchopulmonary C‐fibre endings, but the physiological relevance of this sensitization is unknown. If this exposure augments the reflex responses via a central mechanism, then the responses of higher‐order neurones in the reflex pathway and some components of the reflex output should also be augmented. Guinea‐pigs were chronically exposed to sidestream tobacco smoke (surrogate for environmental tobacco smoke) or filtered air for 5 days week−1 from age 1 to 6 weeks (age equivalent of human childhood) and were then anaesthetized, paralysed, ventilated and prepared with pneumothoraces. Baseline and left atrial capsaicin (0.5 and 2.0 μg kg−1)‐ evoked changes in the impulse activity of vagal C‐fibre‐activated neurones in nucleus tractus solitarii (NTS), phrenic nerve activity, tracheal pressure, arterial blood pressure and heart rate were compared in the two groups. Sidestream smoke exposure significantly augmented the peak (P= 0.02) and duration (P= 0.01) of the NTS neuronal responses and the prolongation of expiratory time (P= 0.003) at the higher capsaicin dose. Thus, the sensitization of the bronchopulmonary C‐fibre endings by chronic exposure to sidestream tobacco smoke is transmitted to the NTS and is associated with a prolonged reflexively evoked expiratory apnoea. The findings may help to explain some related respiratory symptoms in children and be a factor in sudden infant death syndrome.