Effect of Inhaled Furosemide on Cough Response to Citric Acid in Normal Subjects

Author(s):  
M. Robuschi ◽  
A. Vaghi ◽  
G. Gambaro ◽  
S. Spagnotto ◽  
G. Petrigni ◽  
...  
1990 ◽  
Vol 78 (5) ◽  
pp. 521-525 ◽  
Author(s):  
Manuel J. Barros ◽  
Stefano J. Zammattio ◽  
P. John Rees

1. The cough response to inhalation of citric acid is produced mainly by irritation of the larynx and trachea. Variations in the inspiratory flow rate might lead to changes in deposition of the drug, and consequently in the cough threshold. 2. We have studied the effect of three different inspiratory flow rates in 11 normal, non-smoking subjects (nine males, aged 23–39 years), who inhaled nebulized citric acid (2.5–640 mg/l). The test finished when a cough. was produced at each inhalation (cough threshold) or the maximum concentration was reached. 3. The inspiratory flow rate was limited with a fixed resistance and displayed on a screen so that the subjects could reach a constant inspiratory flow rate of 50, 100 and 150 l/min with a submaximal inspiratory effort. 4. The mean (sd) inspiratory flow rates achieved were 51.4 (5.3), 86.2 (16.6) and 134.4 (22.9) l/min. Baseline forced expiratory volume in 1 s and functional vital capacity were not different on the 3 study days. 5. The cough threshold (geometric mean and 95% confidence intervals) was 21 (9–54) mg/l at an inspiratory flow rate of 50 l/min and 43 (13–141) mg/l at 150 l/min (P <0.05). The amount of drug tolerated by the subjects before the cough threshold was achieved was 5.2 (2.0–13.8) mg at an inspiratory flow rate of 50 l/min and 11.6 (3.4–39.8) mg at 150 l/min (P <0.05). The number of coughs per inhalation was 1.6 (1.1–2.0) at an inspiratory flow rate of 50 l/min and 1.1 (0.7–1.5) at 150 l/min (P <0.05). 6. We conclude that lower inspiratory flow rates were associated with a greater cough stimulus in the citric acid challenge procedure used in this study. This may be related to increased laryngeal deposition. The inspiratory flow rate is a variable which should be controlled in the performance of cough challenges with citric acid.


1983 ◽  
Vol 65 (3) ◽  
pp. 53P-53P
Author(s):  
J. Pounsford ◽  
K.B. Saunders
Keyword(s):  

1991 ◽  
Vol 81 (s25) ◽  
pp. 539-542 ◽  
Author(s):  
M. J. Barros ◽  
S. L. Zammattio ◽  
P. J. Rees

1. Twelve non-smoking subjects inhaled capsaicin at three different inspiratory flow rates: 50, 100 and 150 litres/min. Capsaicin was delivered by a breath-actuated dosimeter; inhalations consisted of 0.21–13.6 nmol of capsaicin in doubling amounts given in random order. 2. The mean number of coughs per challenge decreased with increasing inspiratory flow rate. The difference in cough numbers were significant: 7.7 (95% confidence interval 2.5–12.8) for 50 versus 100 litres/min and 10.9 (95% confidence interval 5.0–16.9) for 100 versus 150 litres/min. 3. On a separate day, a cough threshold was measured by giving increasing doses of citric acid that were inhaled at 50 litres/min. There was a positive correlation between the sensitivity to capsaicin and the cough threshold to citric acid (r = 0.69, P = 0.01), and also between the cough latencies (r = 0.67, P = 0.02). 4. The negative relationship between the cough response and the inspiratory flow rate may be caused by increased laryngeal deposition at lower inspiratory flow rates. 5. These results are compatible with a similar anatomical distribution of cough receptors for capsaicin and citric acid. 6. These results suggest that changes in inspiratory flow rate may affect the results of cough challenges.


BMJ ◽  
1986 ◽  
Vol 293 (6561) ◽  
pp. 1528-1528 ◽  
Author(s):  
J C Pounsford ◽  
K B Saunders
Keyword(s):  

1995 ◽  
Vol 79 (4) ◽  
pp. 1082-1087 ◽  
Author(s):  
U. G. Lalloo ◽  
A. J. Fox ◽  
M. G. Belvisi ◽  
K. F. Chung ◽  
P. J. Barnes

Acidic solutions mimick many of the effects of capsaicin (Cap), including pain, bronchoconstriction, cough, and sensory neuropeptide release. Evidence from the use of the Cap antagonist capsazepine suggests that in some cases protons act at the Cap receptor. In the present study, we have investigated whether cough evoked by Cap and citric acid (CA) is mediated specifically via the Cap receptor on airway sensory nerves. We have examined the effects of capsazepine on Cap-, CA-, and hypertonic saline-induced cough and also on CA-induced nasal irritation in awake guinea pigs. Capsazepine was nebulized for 5 min before cough challenges with Cap for 5 min and CA for 10 min. Control animals were pretreated with vehicle alone. Capsazepine (100 microM) inhibited the cough response to 30 microM Cap from 0.77 +/- 0.14 coughs/min in control animals to 0.23 +/- 0.08 coughs/min (P < 0.05) and to 80 microM Cap from 1.4 +/- 0.23 to 0.3 +/- 0.11 coughs/min (P < 0.01). There was no effect, however, of lower concentrations of capsazepine (5 and 10 microM) against Cap-evoked cough. At a concentration of 100 microM, capsazepine also inhibited the coughing induced by 0.25 M CA from 1.8 +/- 0.26 to 0.93 +/- 0.31 coughs/min (P < 0.05) but not that induced by 0.5 M CA. Nasal irritation induced by 0.25 M CA, but not by 0.5 M CA, was also inhibited by capsazepine from 2.47 +/- 0.37 to 0.75 +/- 0.31 nose wipes/min (P < 0.05). This inhibitory effect of capsazepine did not appear to reflect a nonspecific suppression of the cough reflex, since cough evoked by exposure to hypertonic (7%) saline for 10 min was unaffected by pretreatment with capsazepine (100 microM). These data show that capsazepine is a specific inhibitor of Cap- and CA-induced cough in guinea pigs. Moreover, they suggest that low pH stimuli evoke cough and nasal irritation by an action at the Cap receptor, either directly or through the release of an intermediate agent.


1983 ◽  
Vol 65 (3) ◽  
pp. 8P-8P
Author(s):  
J.C. Pounsford ◽  
K.B. Saunders

Thorax ◽  
1994 ◽  
Vol 49 (10) ◽  
pp. 1024-1026 ◽  
Author(s):  
A H Morice ◽  
A E Marshall ◽  
K S Higgins ◽  
T J Grattan
Keyword(s):  

1985 ◽  
Vol 68 (s11) ◽  
pp. 59P-59P
Author(s):  
J.C. Pounsford ◽  
R.N. Davidson ◽  
K.B. Saunders
Keyword(s):  

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