Abstract
The resistance of the larynx to airflow was measured during hypercapnia, hypoxemia, and stimulation of peripheral chemoreceptors by sodium cyanide and phenyl diguanide in 15 dogs anesthetized with α-chloralose (80 mg/kg). Laryngeal airway resistance (R1x) was obtained by measuring the pressure difference between the subglottic region and the mouth while a constant flow of humidified air was passed through the larynx. During spontaneous respiration, R1x varies with the phase of the respiratory cycle: R1x is high during expiration (mean ± SEM = 0.79 ± 0.19 cm H2O/L/sec) and falls just before inspiration (0.49 ± 0.14 cm H2O/L/sec) and remains low until the end of inspiration. Hypercapnia, hypoxemia, and chemoreceptor stimulation each stimulated respiration and simultaneously decreased R1x during both inspiration and expiration. Chemoreceptor stimulation with phenyl diguanide (100 μg/kg) and sodium cyanide (100 μg/kg) produced similar decreases in R1x whether injected into the right atrium or left ventricle, indicating that these agents are not stimulating pulmonary receptors. The decrease in R1x during stimulation of chemoreceptors will decrease the work of ventilation. This study suggests that the control of ventilation involves the active regulation of the resistance of the laryngeal airway.
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