TY - JOUR
T1 - Bronchoconstriction triggered by breathing hot humid air in patients with asthma role of cholinergic reflex
AU - Hayes, Don
AU - Collins, Paul B.
AU - Khosravi, Mehdi
AU - Lin, Ruei Lung
AU - Lee, Lu Yuan
PY - 2012/6/1
Y1 - 2012/6/1
N2 - Rationale: Hyperventilation of hot humid air induces transient bronchoconstriction in patients with asthma; the underlying mechanism is not known. Recent studies showed that an increase in temperature activates vagal bronchopulmonary C-fiber sensory nerves, which upon activation can elicit reflex bronchoconstriction. Objectives: This study was designed to test the hypothesis that the bronchoconstriction induced by increasing airway temperature in patients with asthma is mediated through cholinergic reflex resulting from activation of these airway sensory nerves. Methods: Specific airway resistance (SRaw) and pulmonary function were measured to determine the airway responses to isocapnic hyperventilation of humidified air at hot (49°C; HA) and room temperature (20-22°C; RA) for 4 minutes in six patients with mild asthma and six healthy subjects. A double-blind design was used to compare the effects between pretreatments with ipratropium bromide and placebo aerosols on the airway responses to HA challenge in these patients. Measurements and Main Results:aw increased by 112% immediately after hyperventilation of HA and by only 38% after RA in patients with asthma. Breathing HA, but not RA, triggered coughs in these patients. In contrast, hyperventilation of HA did not cause cough and increased SRaw by only 22% in healthy subjects; there was no difference between their SRaw responses to HA and RA challenges. More importantly, pretreatment with ipratropium completely prevented the HA-induced bronchoconstriction in patients with asthma. Conclusions: Bronchoconstriction induced by increasing airway temperature in patients with asthma is mediated through the cholinergic reflex pathway. The concomitant increase in cough response further indicates an involvement of airway sensory nerves, presumably the thermosensitive C-fiber afferents.
AB - Rationale: Hyperventilation of hot humid air induces transient bronchoconstriction in patients with asthma; the underlying mechanism is not known. Recent studies showed that an increase in temperature activates vagal bronchopulmonary C-fiber sensory nerves, which upon activation can elicit reflex bronchoconstriction. Objectives: This study was designed to test the hypothesis that the bronchoconstriction induced by increasing airway temperature in patients with asthma is mediated through cholinergic reflex resulting from activation of these airway sensory nerves. Methods: Specific airway resistance (SRaw) and pulmonary function were measured to determine the airway responses to isocapnic hyperventilation of humidified air at hot (49°C; HA) and room temperature (20-22°C; RA) for 4 minutes in six patients with mild asthma and six healthy subjects. A double-blind design was used to compare the effects between pretreatments with ipratropium bromide and placebo aerosols on the airway responses to HA challenge in these patients. Measurements and Main Results:aw increased by 112% immediately after hyperventilation of HA and by only 38% after RA in patients with asthma. Breathing HA, but not RA, triggered coughs in these patients. In contrast, hyperventilation of HA did not cause cough and increased SRaw by only 22% in healthy subjects; there was no difference between their SRaw responses to HA and RA challenges. More importantly, pretreatment with ipratropium completely prevented the HA-induced bronchoconstriction in patients with asthma. Conclusions: Bronchoconstriction induced by increasing airway temperature in patients with asthma is mediated through the cholinergic reflex pathway. The concomitant increase in cough response further indicates an involvement of airway sensory nerves, presumably the thermosensitive C-fiber afferents.
KW - Asthma
KW - Bronchoconstriction
KW - Cough
KW - Ipratropium
KW - TRPV1
UR - http://www.scopus.com/inward/record.url?scp=84861790702&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=84861790702&partnerID=8YFLogxK
U2 - 10.1164/rccm.201201-0088OC
DO - 10.1164/rccm.201201-0088OC
M3 - Article
C2 - 22505744
AN - SCOPUS:84861790702
SN - 1073-449X
VL - 185
SP - 1190
EP - 1196
JO - American Journal of Respiratory and Critical Care Medicine
JF - American Journal of Respiratory and Critical Care Medicine
IS - 11
ER -