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Effect of Inspiratory Flow Rate on Bronchomotor Tone in Normal and Asthmatic Subjects

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Effect of Inspiratory Flow Rate on Bronchomotor Tone in Normal and Asthmatic Subjects Thorax: first published as 10.1136/thx.39.2.86 on 1 February 1984. Downloaded from Thorax 1984;39:86-92 Effect of inspiratory flow rate on bronchomotor tone in normal and asthmatic subjects W HIDA, M ARAI, C SHINDOH, Y-N LIU, H SASAKI, T TAKISHIMA From the First Department ofInternal Medicine, Tohoku University School of Medicine, Sendai, Japan ABSTRACT The effect of the inspiratory flow rate during deep inspiration on the regulation of bronchomotor tone was studied in nine normal and 22 asthmatic subjects. Changes in bronchial tone were assessed by respiratory resistance measured by an oscillation method. In normal subjects with bronchoconstriction induced by methacholine a rapid deep inspiration reduced respiratory resistance more than a slow deep inspiration. Asthmatic subjects with spontaneous airway narrowing showed an increase in respiratory resistance after deep inspiration that was greater after rapid than after slow deep inspiration. On the other hand, in asthmatics with methacholine induced bronchoconstriction, bronchodilatation occurred after deep inspiration and this was also greater after rapid than after slow deep inspiration. Lignocaine inhalation attenuated both bronchoconstriction and bronchodilatation induced by both slow and rapid deep inspiration. These results suggest that the effects of deep inspiration are mediated at least in part via receptors in the airways. It is suggested that in asthmatic patients with spontaneous broncho- constriction irritant receptor activity will be increased in proportion to the speed of inspiration. After methacholine induced bronchoconstriction stretch receptor activity is likely to behave in a similar fashion, leading to an opposite effect. http://thorax.bmj.com/ A deep inspiration has been reported to produce a carbachol induced bronchoconstriction, and they transient decrease in airway calibre in some asthma- suggested that this might have been due to greater tic subjects.' 2 In contrast, in the presence of phar- stimulation of stretch receptors at higher flows. macologically induced bronchoconstriction a deep The inspiratory flow has not been controlled in inspiration produces bronchodilatation in most previous studies reporting bronchoconstriction asthmatice and normal4 subjects. The reason for induced by deep inspiration.' 2 We therefore these divergent effects of deep inspiration on bron- examined whether the flow rate during a deep inspi- chomotor tone with and without drug induced ration affects bronchomotor tone in asthmatic bronchoconstriction is unclear. Deep inspiration patients with drug induced bronchoconstriction and on October 2, 2021 by guest. Protected copyright. might stimulate different vagal sensory receptors in with spontaneous bronchomotor tone. In addition, these different circumstances: in those with artifi- we examined the effects of rate of deep inspiration in cially induced bronchoconstriction deep inspiration asthmatic and normal subjects after pretreatment might stimulate stretch receptors, which induce with lignocaine, which is known to block both irrit- bronchodilatation5; while in asthmatics without pro- ant and stretch receptors.8 We also examined voked bronchoconstriction deep inspiration might whether any bronchoconstrictor effect of the speed activate irritant receptors, inducing broncho- of inspiratory flow was related to the degree of air- constriction.6 Recently, Beaupre and Orehek' way hypersensitivity as assessed by sensitivity to observed that a fast inspiratory flow rate induced methacholine. more bronchodilatation than after inspiration with a slow inspiratory flow rate in asthmatic subjects with Methods We studied nine normal men (mean age 28-8 (SEM Address for reprint requests: Dr Tamotsu Takishima, First 1.7) years) and 22 patients with asthma (16 men and Department of Internal Medicine, Tohoku University School of six women, mean age 38-8 (3.4) years) who were Medicine, Sendai, Japan 980. diagnosed on clinical and functional criteria.9 None Accepted I November 1983 was having long term steroid treatment. All were 86 Thorax: first published as 10.1136/thx.39.2.86 on 1 February 1984. Downloaded from Inspiratory flow rate and bronchomotor tone in normal and asthmatic subjects 87 symptomless at the time of study, and no medication analysis. Then during tidal breathing each normal was taken for at least 24 hours before the study. subject continuously inhaled an aerosol of a single Initially the vital capacity (VC) and the forced concentration of methacholine (6.25 mg/ml) for expiratory volume in one second (FEV,) were about six minutes until the Rrs was twice the initial measured with a 13*5 litre Benedict-Roth spirome- value. After inhalation of methacholine FRC usually ter. Predicted values of VC were obtained from the increased by 0S4-07 1. Rrs after slow and rapid deep data of Cotes.'0 About one hour later the effects of inspiration was then measured again as described deep inspiration were examined with the subject above. seated in a volume displacement body plethysmo- In the asthmatic subjects the effects of slow and graph"; the respiratory resistance (Rrs) was meas- rapid deep inspiration on baseline Rrs were studied ured by the oscillation technique,'2 while the volume in the same way as in the normal subjects. In 13 of change within the plethysmograph was monitored the 22 asthmatic subjects, the studies were repeated by a Krogh spirometer and Sanborn linear trans- after methacholine (6.25 mg/ml) had been inhaled ducer. A sine wave of frequency 3 Hz was generated for about one minute-that is, until there had been a at the mouth by a loudspeaker box system.'2 The twofold increase in Rrs. This increased FRC by mouth pressure relative to ambient pressure was 0-5-0 8 litre. measured with a differential pressure transducer To examine the contribution of airway sensory (Validyne, MP45 ± 50 cm H20) and air flow at the receptors to the effects of different rates of inspirat- mouth (V) with a Fleisch pneumotachograph and ory flow, studies were also performed (after the air- differential transducer (Validyne, MP45 ± 5 cm ways had been anaesthetised) in four normal sub- H20). The calculation of respiratory resistance from jects with methacholine induced broncho- Pao and V was continuously performed by an constriction and four asthmatic subjects who had analogue computer using the method of Hyatt et transient bronchoconstriction after deep inspira- al.'3 To deliver an aerosol of a bronchoconstrictor tion.8 An aerosol of 4% lignocaine was administered or bronchodilator, two Vaponephrin nebulisers to these subjects with the nebuliser described above (USV Pharmaceutical Corporation) that delivered over a 15 minute period during tidal breathing with 0-15 ml of solution per minute were connected bet- continuous monitoring of Rrs, which showed that ween the mouthpiece and pneumotachograph. A lignocaine itself had no measurable effect. At the constant bias flow of 0-4 1 s-' was introduced bet- end of the measurement the subject inhaled five ween the mouthpiece and the nebuliser to minimise deep breaths of an aerosol of 10% citric acid and the http://thorax.bmj.com/ dead space ventilation. Mouth flow, mouth pressure, absence of cough confirmed the adequacy of airway volume change, and respiratory resistance were anaesthesia.'4 recorded on a four channel direct writing recorder In additional experiments 12 of the 22 asthmatic system (Sanei, Japan). subjects had a methacholine provocation on a sepa- For assessment of the effect of flow rate during rate occasion three or four days later. Nine in this deep inspiration in normal subjects, the protocol group belonged to the group in which the flow was as follows. After functional residual capacity effects of deep inspiration had been studied after (FRC) became steady the subject inspired fully from methacholine induced bronchoconstriction as FRC to total lung capacity (TLC) and expired again described above. Methacholine provocation tests in on October 2, 2021 by guest. Protected copyright. to FRC with either a slow deep inspiration (SDI, these additional studies were performed by a previ- mean flow 0-22 (SEM 0.02) 1 s-') or a rapid deep ously reported technique,'5 which allows construc- inspiration (RDI, mean flow 3-62 (0-22) 1 s-'). The tion of dose response culves of Rrs during the con- flow during expiration from TLC to FRC was com- tinuous inhalation of methacholine in stepwise parable to that during inspiration with each man- incremental concentrations from 0-049 to 25-0 oeuvre. Slow and rapid deep inspirations were per- mg/ml. Rrs was again measured by the oscillation formed in random order. FRC values before and method as described above. From the dose response after each deep inspiration were within 0-2 1 of each curve we obtained the cumulative dose of other. Respiratory resistance was measured con- methacholine (Dmin) required to initiate a decrease tinuously for at least two minutes before each man- in respiratory conductance (Grs, reciprocal of oeuvre and for five minutes afterwards. Further respiratory resistance). Dmin was used as the index deep inspirations were performed at intervals of of bronchial sensitivity and expressed in units, as in about 10 minutes, when respiratory resistance had the work of Chai et al'6-that is, one unit represents returned to its baseline value before deep inspira- the inhalation for one minute of an aerosol of 1-0 tion. The effects of slow and rapid deep inspiration mUml during tidal breathing.'5 We then looked at were each examined two or three times, and average the effects of slow and rapid deep inspiration on values of respiratory resistance were used for respiratory resistance without drug induced Thorax: first published as 10.1136/thx.39.2.86 on 1 February 1984. Downloaded from 88 Hida, Arai, Shindoh, Liu, Sasaki, Takishima Pulmonary function in normal and asthmatic subjects (means with SEM in parentheses) No ofsubjects VC (% predicted) FEV,/VC % Rrs (SD) (SD) (cm H20 1 s) Normal 9 107.9 (5.5) 87.3 (1-2) 2-58 (0-18) Bronchial asthma 22 103-8 (2-3) 72-2 (3-0) 3-42 (0-15) p NS < 0-01 < 0.01 VC-vital capacity; FEV,-forced expiratory volume in one second; Rrs-respiratory resistance; NS-not significant.
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