Laryngeal constriction produced by capsaicin in the cat

Abstract

Pulmonary chemoreflex induced by an intravenous injection of capsaicin in cats consists of prompt apnoea, bradycardia and hypotension, followed by rapid, shallow breathing. The present study was designed to ascertain how much the post-capsaicin arrest of respiration and resumed breathing of pulmonary chemoreflex are contributed by the respiratory laryngeal resistance and by the sensory input from the larynx. The effects of intravenous injection of capsaicin at the dose of 0.01 mg per kg of body weight were studied in eleven anaesthetized cats, breathing spontaneously via tracheal cannula, while the larynx was isolated in situ. In post-capsaicin apnoea the expiratory laryngeal resistance rose four fold compared to pre-challenge values. In the initial and subsequent phase of resumed breathing, the expiratory laryngeal resistance reverted to a value not significantly different from control. With the onset of tachypnoea significant decrease in tidal volume coupled with increased respiratory rate failed to effect minute ventilation. Bilateral section of the superior laryngeal nerve neither prevented laryngeal constriction in apnoea nor the ventilatory effects of capsaicin. Thus laryngeal afferents run within the superior laryngeal nerve are not essential for the respiratory phenomena induced by capsaicin. Midcervical vagotomy performed in six cats abolished the respiratory effect of capsaicin.