The mechanism of aerosol-induced bronchoconstriction.
To gain insight into the mechanism of aerosol induced bronchoconstriction the differences between ultrasonically-nebulized aqueous-induced bronchoconstriction and cough are contrasted. Both normal subjects and asthmatics cough in response to inhalation of aerosol low in chloride ions (Cl-). This is putatively a result of stimulation of rapidly-adapting receptors (RARs). Normals do not develop bronchoconstriction as a result of inhalation of aqueous aerosols. Asthmatics however do but only when the tonicity is increased above or below normal; (Cl-) is not important. Inhaled lignocaine inhibits cough but not bronchoconstriction whilst sodium cromoglycate (SCG) inhibits bronchoconstriction but not cough. As SCG may inhibit vagal C-fibre receptors it is possible that different vagal afferent receptors are involved in cough and bronchoconstriction. Small but significant bronchodilatation in normals attenuates aerosol-induced cough which can be explained by central modulation of medullary cough neurones by slowly-adapting receptors (SARs). As the same occurs with reflex bronchoconstriction, a complex organisation of vagal afferents can be suggested, where different receptors are responsible for cough and bronchoconstriction and SAR activity modulates the medullary neurones which initiate the two reflexes.
Higenbottam
T
T
Regional Respiratory Physiology Laboratory, Papworth Hospital, Cambridge, UK.
D000336:Aerosols; D001980:Bronchi / Q000294:innervation / Q000503:physiopathology*; D001993:Bronchodilator Agents / Q000627:therapeutic use; D003251:Constriction, Pathologic; D003371:Cough / Q000188:drug therapy / Q000503:physiopathology*; D006801:Humans; D011984:Sensory Receptor Cells; D014630:Vagus Nerve / Q000503:physiopathology
D000336:Aerosols; D001993:Bronchodilator Agents