A single deep inspiration (DI) is commonly followed by transient airflow obstruction in asthmatic patients. In some patients, however, DI results in a sustained response which suggests that more than one mechanism may be responsible. We have studied the characteristics of the response to repeated DI, and their modification by various pharmacological agents, by measuring specific airway resistance (sRaw) in ten subjects who showed reproducible and consistent increases in sRaw after DI.

A B S T R A C T Our purpose was to determine whether exposure to a realistic concentration of nitrogen dioxide (NO2) could increase the bronchial sensitivity of asthmatic patients to bronchoconstrictor agents. We established dose-response curves for changes in specific airway resistance (SRaw) in response to aerosolized carbachol in 20 asthmatics after each had spent 1 h in an exposure chamber breathing on one occasion unpolluted air and on a separate occasion 0.1 ppm N02: sequence of exposures to unpolluted air and to low levels of NO2 were randomized in a single-blind fashion. N02 induced a slight but significant increase in initial SRa. and enhanced the bronchoconstrictor effect of carbachol in 13 subjects: curves were shifted to the left and the mean dose of carbachol producing a twofold increase in initial SRaw was decreased from 0.66 mg to 0.36 mg (P < 0.001). In contrast, NO2 neither modified the initial SRaw nor the bronchoconstrictor effect of carbachol in seven subjects. In 4 out of the 20 subjects, exposure to a higher concentration of NO (0.2 ppm) yielded variable results.Potentiation of the carbachol bronchoconstrictor response by NO2 could not be related to any physical or clinical characteristics of the subjects tested. Although the mechanisms underlying the N02 effect remain controversial, the present results demonstrate that very low levels of NO. can adversely affect some asthmatics.

SummaryCumulative dose-response curves to carbachol given by aerosol were established using plethysmographic measurements of specific airways resistance (SRaw) in 10 patients with asthma and five healthy subjects. Two experiments were performed-a control test and one in which maximal respiratory manoeuvres (MRM) (two maximal inspirations and two maximal expirations) were made before each carbachol inhalation. MRM did not modify the dose-response curves in the normal subjects. In the patients these manoeuvres enhanced the bronchoconstrictor effect of carbachol: curves were shifted to the left and the mean dose of carbachol producing a twofold increase in initial SRaw was decreased from 0 373 mg to 0 189 mg (P <0 001). Bronchial provocation tests using methods which require MRM-for example, forced expiratory volume at one second-could overestimate the bronchial sensitivity of patients with asthma.

(1975). Thorax, 30,[657][658][659][660][661][662] Beta-adrenergic function in airways of healthy and asthmatic subjects. We measured the short-term effects of beta-adrenergic blockade with propranolol (0-2 mg/kg iv), followed by stimulation with salbutamol (200 ,ug inhaled), on specific airway conductance (SGaw), heart rate, and systemic blood pressure (BP) in 11 healthy subjects, and 11 symptom-free asthmatics with normal lung function values.Propranolol induced a significant bronchoconstrictor effect in both groups, stronger in asthmatics than in normals: mean SGaw decreased 34-6-4-25% against 9-4±+-9% (P<0-01). Six of the 11 asthmatics exhibited a more pronounced bronchoconstriction than the most responsive healthy subject. Large individual variations were seen in both groups although they were greater in the asthmatics. A similar rise in SGaw was produced by salbutamol in both groups. The decrease of heart rate provoked by propranolol was similar in the two groups, averaging 18-6%, with no further change after salbutamol. The blood pressure was slightly decreased by propranolol in both groups.The results indicate that normal subjects have a weak and variable bronchodilator beta-adrenergic activity. In most asthmatics beta-adrenergic tone appeared more pronounced. The individual differences in response to propranolol observed in both groups suggest that asthmatic patients differ quantitatively rather than qualitatively from healthy subjects with respect to beta-adrenergic receptor function. There was no association between clinical findings and the degree of bronchomotor effect of propranolol in the patients with asthma. This study does not support the view that airways of asthmatic patients have a decreased beta-adrenergic receptor function.

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