Airway anesthesia and respiratory response to methylcholine induced bronchoconstriction.
P0.1 and breathing pattern in response to acute methylcholine induced bronchoconstriction were studied with and without previous airway anesthesia in 6 normal subjects. In a randomized cross-over study, on two successive days, the subjects inhaled either 4% lidocaine hydrochloride or isotonic saline for 12 min, and then methylcholine for 3 min. FEV1, P0.1, and breathing patterns were measured at baseline and following each inhalation. Baseline values were changed neither by saline, nor by lidocaine, and methylcholine induced the same 18% decrease in FEV1 after each agent. Bronchospasm was not accompanied by a change in PACO2. After saline, methylcholine bronchospasm was associated with an increase of P0.1 from 1.0 +/- 0.2 (SEM) to 1.8 cm H2O +/- 0.3 (SEM) (P less than 0.05). During bronchospasm following airway anesthesia. P0.1 was increased from 1.1 +/- 0.2 (SEM) to 1.3 cm H2O +/- 0.3 (SEM), which was not significant. Comparing bronchospasm after saline to that after xylocaine we observed an increase in Ti afer xylocaine, which was correlated with the decrease in P0.1, suggesting that both were affected by airway anesthesia. We concluded that vagal airway receptors contribute to the increase in inspiratory drive which accompanies acute bronchospasm and also may contribute to the regulation of resting breathing pattern during bronchospasm in humans.
D000328:Adult; D000770:Anesthesia, Endotracheal; D001986:Bronchial Spasm / Q000139:chemically induced / Q000503:physiopathology*; D002794:Choline / Q000009:adverse effects / Q000031:analogs & derivatives; D006801:Humans; D012119:Respiration; D013997:Time Factors
C017506:methylcholine; D002794:Choline