It has been hypothesized that bronchoconstriction due to exercise and hyperventilation is caused by the stimulation of irritant receptors in the upper airways. However, controversial results have been reported on the effect of lignocaine, which can inhibit the stimulation of these receptors. The aim of this study was to investigate the effect of inhaled lignocaine on bronchial responsiveness to hyperventilation of cold dry air in asthmatic subjects. Eight adult asthmatic subjects in a clinical steady state came on four different days (two placebo and two active days in random order) with a maximum interval of 3 weeks. After assessment of forced expiratory flow rates, inhalation of either phosphate-buffered saline (placebo) or lignocaine solution (40 mg) was carried out in a single-blind fashion. The technician was not aware which medication was being inhaled, but the asthmatic subject knew which drug it was by the sensation in his or her throat. Forced expiratory flow rates were reassessed 15 min after the nebulization; then, the subjects were asked to inhale cold dry air (-20 degrees C) in progressively increasing levels of ventilation (7.5, 15, 30 and 60 l/min and maximum voluntary ventilation). PD20 was interpolated from the dose-response curve, relating the dose of cold air on a non-cumulative logarithmic scale on the abscissa and the percentage change in FEV1 on the ordinate. There were no significant changes in FEV1 and PD20 after inhalation of lignocaine as compared to the placebo. We conclude that inhaled lignocaine does not significantly alter bronchial hyperresponsiveness to hyperventilation of cold air in asthmatic subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

We investigated the effects of particles of sawdust delivered through a special device at known concentrations (close to the threshold limit value-short term exposure limit (TLV-STEL) of 10 mg.m-3) on FEV1 and PC20 in 12 asthmatic subjects free of clinical sensitization to this product. Subjects were studied over two days (day 1: exposure to sawdust; day 2: sham exposure) in random order with a maximum interval of 1 week. On each day, after the assessment of spirometry and PC20, subjects underwent exposure to sawdust or sham exposure. Sawdust was inhaled for a total of 30 min at average concentrations varying from 8.0 to 19.3 mg.m-3 (mean = 11.5 mg.m-3). Twenty-five to 39.7% (mean = 34.6%) of inhaled particles had a diameter less than 10 mu (diameter allowing deposition in the trachea and lower respiratory tract). At the end of each period of exposure, FEV1 was assessed. After recovery, the second PC20 was obtained. Serial measurements of FEV1 were carried out every hour for up to 6 h after the end of exposure. At that time, PC20 was reassessed. Only one subject showed an acute bronchoconstriction immediately after exposure to sawdust (maximum fall of 14% in FEV1) with complete recovery 10 min later. Overall, inhalation of sawdust did not modify PC20 by comparing the mean result of the first test with the second and the third assessments. Also, the mean changes in PC20 at each interval after exposure to sawdust were not significantly different from the variations in PC20 on the sham day.(ABSTRACT TRUNCATED AT 250 WORDS)

Hyperventilation of cold dry air causes bronchoconstriction in asthmatic subjects and has been proposed as a test for assessing bronchial hyperresponsiveness. The influence of the duration of inhalation of unconditioned cold air has not been studied. We have investigated the question in 12 asthmatic subjects in a clinically stable state. Each subject underwent three inhalation tests at a maximum interval of two weeks. On each day, the duration of inhalation was different, being randomly 2, 3 or 4 min depending on the subject. Doubling doses of cold air produced by a freon conditioner were administered, increasing ventilation from 7.5 to 15, 30, 60 l.min-1 and maximum voluntary ventilation (MVV). Forced expiratory volume in one second (FEV1) was assessed after each period of cold air inhalation. The test was stopped when the FEV1 had decreased by 20% or more, or when MVV had been achieved. The dose of cold air expressed as the level of ventilation causing a 20% change in FEV1 (PD20) was interpolated from individual dose-response curves. Dose-response curves shifted to the left when the duration of ventilation was increased. PD20 was significantly lower after 3 min of ventilation than after 2 min (mean +/- SD PD20 of 41.7 +/- 1.4 l.min-1 compared with 53.3 +/- 1.2 l.min-1; p = 0.002). There was a further fall in PD20 after 4 min of ventilation (PD20 = 36.1 +/- 1.5 l.min-1) but the difference compared with the values obtained after 3 min was not significant (p = 0.09), thus suggesting a plateau.(ABSTRACT TRUNCATED AT 250 WORDS)

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