Cooling of the upper airway, which stimulates specific cold receptors and inhibits laryngeal mechanoreceptors, reduces respiratory activity in unanesthetized humans and anesthetized animals. This study shows that laryngeal cooling affects the pattern of breathing in the guinea pig and assesses the potential role of cold receptors in this response by using a specific stimulant of cold receptors (l-menthol). The response to airflows (30 ml/s, 10-s duration) through the isolated upper airway was studied in 23 anesthetized (urethan, 1 g/kg ip) guinea pigs breathing through a tracheostomy. Respiratory airflow, tidal volume, laryngeal temperature, and esophageal pressure were recorded before the challenges (control), during cold airflows (25 degrees C, 55% relative humidity), and during warm airflows (37 degrees C, saturated) with or without the addition of l-menthol. Whereas warm air trials had no effect, cold air trials, which lowered laryngeal but not nasal temperature, reduced ventilation (VE) to 85% of control, mainly by prolonging expiratory time (TE, 145% of control), an effect abolished by laryngeal anesthesia. Addition of l-menthol to the warm airflow caused a greater reduction in VE (41% of control) by prolonging TE (1,028% of control). Nasal anesthesia markedly reduced the apneogenic effect of l-menthol but did not affect the response to cold air trials. In conclusion, both cooling of the larynx and l-menthol in the laryngeal lumen reduce ventilation. Exposure of the nasal cavity to l-menthol markedly enhances this ventilatory inhibition; considering the stimulatory effect of l-menthol on cold receptors, these results suggest a predominant role of nasal cold receptors in this response.
In anesthetized cats, we examined cardiorespiratory activity during excitation of large afferent fibers from muscle proprioceptors. We found that selective stimulation of group I fibers with electric impulses at 200-300 Hz induces an increase in pulmonary ventilation from control value (mean +/- SE) of 486 +/- 8 to a maximum of 544 +/- 8 ml/min and an increase in mean systemic arterial pressure from control value of 151 +/- 2 to a maximum of 160 +/- 2 mmHg. Neither of these increases was produced by the same stimulation when applied during anodal block of volleys of group I fibers. Hyperpnea could be obtained independently from changes in cardiovascular activity, and the pressor response could be obtained during artificial ventilation at constant tidal volume after curarization. Consequently, it appears that respiratory and cardiovascular responses to stimulation of group I fibers can be independent of each other.
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