Occlusion pressure in acute bronchospasm induced by methylcholine.
We measured resting minute ventilation, the pressure developed by the inspiratory muscles during the first 0.1 sec of inspiratory effect against an occluded airway (P0.1), FRC and airway resistance in normal subjects during bronchoconstriction induced by methylcholine inhalation and again after the bronchoconstriction had been reversed by inhaled isoproterenol. Methylcholine resulted in a 2- to 3-fold increase in airway resistance, FRC rose in 5/6 subjects and ventilation changed in variable fashion. P0.1 increased in all subjects with methylcholine and decreased after isoproterenol. When the subjects were considred as a group, P0.1 correlated positively with airway resistance. Normal subjects respond to bronchoconstriction as they do to external resistance loading, by increasing inspiratory muscle activity. During bronchoconstriction, all subjects demonstrated an increase of breathing frequency and a decrease in the duration of expiration; inspiratory duration did not change significantly. This response may have been due to activity of pulmonary irritant receptors. Breathing frequency and expiratory duration returned to control levels with isoproterenol, so we could not show that this response was independent of changes in lung mechanics.
D000328:Adult; D000403:Airway Resistance; D001986:Bronchial Spasm / Q000139:chemically induced / Q000503:physiopathology*; D005260:Female; D005652:Functional Residual Capacity; D006801:Humans; D007545:Isoproterenol / Q000494:pharmacology; D008168:Lung / Q000503:physiopathology*; D008297:Male; D008688:Methacholine Compounds
D008688:Methacholine Compounds; D007545:Isoproterenol