A reassessment of the effects of oropharyngeal anesthesia in exercise-induced asthma.
To investigate the possibility that stimulation of neural receptors in the posterior pharynx plays a role in the pathogenesis of exercise-induced asthma, we had 10 asthmatic subjects simulate the hyperpnea of exercise by performing eucapnic hypervenilation in the presence and absence of oropharyngeal anesthesia induced by lidocaine. During these studies, the amount of ventilation and temperature and water content of the inspired air were rigorously controlled in order to keep respiratory heat loss constant for each trial. Multiple aspects of pulmonary mechanics were measured before and after the pharynx was sprayed with either water or lidocaine, as well as after the completion of the bronchial challenge. Neither agent, in and of itself, produced alterations in lung function at rest. Eucapnic hyperventilaltion was followed by a significant reduction in pulmonary mechanics in both situations, and there were no significant differences between the effects of lidocaine or water. Thus, we were unable to find any evidence for the existence of "irritant-like" receptors essential to the pathogenetic consequences of airway cooling in the posterior pharynx.
D000328:Adult; D001249:Asthma / Q000139:chemically induced*; D001250:Asthma, Exercise-Induced / Q000139:chemically induced* / Q000209:etiology; D004525:Efferent Pathways / Q000502:physiology; D005260:Female; D005541:Forced Expiratory Volume; D006801:Humans; D008012:Lidocaine / Q000494:pharmacology; D008297:Male; D009960:Oropharynx / Q000187:drug effects / Q000294:innervation*; D010991:Plethysmography; D011984:Sensory Receptor Cells / Q000502:physiology; D013147:Spirometry
D008012:Lidocaine