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Query: UMLS:C0010200 (cough)
23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We have studied cough and bronchial constriction induced by inhaling citric acid in 15 smokers with baseline airflow obstruction, in 13 occasional smokers and 13 non smokers. The threshold for cough was significantly higher in occasional smokers in relation to smokers and non smokers. Citric acid produced the same degree of bronchial constriction at the same time in smokers and occasional smokers: the maximum fall in forced expired volume (FEV1-VEMS) was recorded five seconds after inhalation of the citric acid (dose threshold) and there was no significant difference between the two groups. In the non smokers, the maximum fall in VEMS was recorded twenty seconds after inhalation of the citric acid and was significantly less in relation to that of the smokers and occasional smokers. In the smokers the degree of smoking could influence the fall of VEMS (% predicted). Cough and bronchial constriction after the inhalation of citric acid are probably related to different physiological mechanisms and are linked to the history of smoking.
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PMID:[Cough and bronchial obstruction induced by citric acid in smokers, occasional smokers and non-smokers]. 192 77

The relation between citric acid cough threshold and airway hyperresponsiveness was investigated in 11 non-smoking patients with allergic asthma (mean FEV1 94% predicted) and 25 non-atopic smokers with chronic airflow obstruction (mean FEV1 65% predicted). Cough threshold was determined on two occasions by administering doubling concentrations of citric acid. Seven of the 11 asthmatic subjects and 14 of 25 smokers with chronic airflow obstruction had a positive cough threshold on both test days. Cough threshold measurements were reproducible in both groups (standard deviation of duplicate measurements 1.2 doubling concentrations in asthma, 1.1 doubling concentrations in chronic airflow obstruction). Citric acid provocation did not cause bronchial obstruction in most patients, though four patients had a fall in FEV1 of more than 20% for a short time on one occasion only. No significant difference in cough threshold was found between the two patient groups despite differences in baseline FEV1 values. There was no significant correlation between cough threshold and the provocative concentration of histamine causing a 20% fall in FEV1 (PC20) histamine in either group. Thus sensory nerves can be activated with a tussive agent in patients with asthma and chronic airflow obstruction without causing bronchial smooth muscle contraction.
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PMID:Citric acid cough threshold and airway responsiveness in asthmatic patients and smokers with chronic airflow obstruction. 194 92

Delapril, a nonsulfhydryl angiotensin converting enzyme (ACE) inhibitor, which has an indanylglycine moiety differing from the proline moiety of captopril or enalapril, is an esterified prodrug that is converted in vivo to its active metabolites. Delapril effectively inhibits rabbit lung ACE activity and lowers blood pressure in spontaneously hypertensive rats. Delapril has several characteristics that differ from captopril and enalapril, including high lipophilicity and weak bradykinin potentiating action. Delapril is a more potent inhibitor of vascular wall ACE activity than enalapril or captopril. It also shows a weaker potentiating action on the citric acid-induced cough in the guinea pig model compared with captopril and enalapril. In 12 out of 150 patients with essential hypertension who complained of cough during treatment with enalapril, changing to delapril resulted in resolution of the cough in 6 out of 12 of these patients: the percentage of patients in the total population with cough decreased from 8% to 4%.
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PMID:Characteristics of a new angiotensin converting enzyme inhibitor: delapril. 200 44

To compare the effects of three different angiotensin converting enzyme (ACE) inhibitors on the cough reflex, capsaicin and citric acid challenge tests were done in normal subjects and hypertensive patients before and after administration of delapril, captopril, or enalapril. Two groups of 7 normal subjects (single dose study: 15 mg delapril v 18.75 mg captopril or 2.5 mg enalapril) and a group of 6 mildly hypertensive patients (1 week study: cross-over administration of 30 mg/day delapril, 37.5 mg/day captopril, or 5 mg/day enalapril) were studied. Another group of 6 patients with essential hypertension was treated with three ACE inhibitors for 4 weeks in a randomized order, with a 2 week washout period between active therapies. Aerosols of 1 mumol/L and 3 mumol/L capsaicin and 0.68% citric acid in 0.9% NaCl were generated by an ultrasonic nebulizer, and the frequency of cough was counted during inhalation. Delapril treatment resulted in substantially fewer patients with a significant increase (greater than or equal to 4 coughs during treatment than during the control period) in the frequency of cough than did captopril treatment. In the 1 and 4 week studies, enalapril and captopril had substantially more occurrences of significantly increased capsaicin-induced cough than did delapril. These results indicate that delapril has the least cough stimulatory effect among these ACE inhibitors, which may be clinically beneficial.
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PMID:Comparative study of the effects of three angiotensin converting enzyme inhibitors on the cough reflex. 200 48

Inhaled corticosteroids are known to reduce respiratory symptoms and airway responsiveness in allergic patients with asthma. The aim of the present randomised, double blind study was to assess the effect of eight weeks' treatment with inhaled budesonide in non-allergic smokers with chronic obstructive lung disease. Twenty four subjects (23 male) entered the study. Their ages ranged from 40 to 70 (mean 57) years, with a mean of 35 (range 9-80) pack years of smoking; the mean FEV1 was 53% (range 32-74%) predicted and geometric mean PC20 (histamine concentration causing a 20% fall in FEV1) 0.96 (range 0.07-7.82) mg/ml. After a two week washout, single blind, placebo period, 12 patients were allocated to treatment with budesonide 1600 microgram/day and 12 to placebo for eight weeks. The only additional drug to be taken was ipratropium bromide "if needed." Twenty one patients completed the study, 10 in the budesonide group and 11 in the placebo group. The standard deviation of the difference between duplicate measurements of PC20 histamine and citric acid cough threshold made two weeks apart was below one doubling dose step. There was a significant reduction in dyspnoea in the budesonide group, but otherwise no change in symptom scores or use of ipratropium bromide over the eight weeks of treatment within or between the two groups. No significant differences in spirometric values, peak expiratory flow, PC20 histamine, or citric acid cough threshold were found between the groups. Although differences were not significant, some of the changes showed a trend in favour of budesonide. Whether a longer observation period would show a significant influence of inhaled corticosteroids in patients with chronic obstructive lung disease remains to be determined.
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PMID:Effects of inhaled budesonide on spirometric values, reversibility, airway responsiveness, and cough threshold in smokers with chronic obstructive lung disease. 206 95

Effects of opioids and opioid antagonists on citric acid-induced cough and reflex bronchoconstriction have been examined in conscious guinea pigs. Airway reflexes produced by inhaled citric acid are mediated by capsaicin sensitive sensory neurons, and we examined particularly the possibility that inhibitory effects of opioids can be exerted locally in the airway. As expected, systemically administered codeine (1-10 mg/kg), meperidine (3-30 mg/kg) and morphine (1-10 mg/kg) dose-dependently inhibited cough and bronchoconstriction. However, inhalations of nebulized codeine (10-100 mg/ml) and morphine (10-30 mg/ml) also produced these effects. The potency and rapid onset of action of inhaled codeine suggest that it exerted its effects without first being metabolized to morphine. The opioid receptor antagonist naloxone completely (10-100 micrograms/kg), and nalorphine (a mixed agonist/antagonist) (1-3 mg/kg) partly, inhibited codeine's antitussive and antibronchoconstrictor effects. Nalorphine alone (3-30 mg/kg) inhibited citric acid induced reflexes, whereas naloxone was without effect. Prior inhalation of a quaternary opioid receptor antagonist, levallorphan methyl iodide (10 mg/ml), abolished the inhibitory effects of inhaled codeine (30 mg/ml). The present data suggest that inhibition of cough and reflex bronchoconstriction can be produced by opioids, acting on mu and kappa receptors located in the guinea pig tracheobronchial tree. The possible existence in the airways of a unique opioid receptor mediating inhibition of cough (as described in the central nervous system) cannot be excluded.
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PMID:Airway opioid receptors mediate inhibition of cough and reflex bronchoconstriction in guinea pigs. 215 65

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 less than 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 less than 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 less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Importance of inspiratory flow rate in the cough response to citric acid inhalation in normal subjects. 216 81

The effect of upper abdominal surgery under general anaesthesia on the cough threshold was studied in 26 patients, on the basis of the concentrations of capsaicin and citric acid causing cough. Cough threshold was determined after administering doubling doses of nebulised aerosols of capsaicin and citric acid before operation and on the first and fourth postoperative days. There was an increase in cough threshold (decrease in cough sensitivity) in response to both inhaled irritants on the first postoperative day from the preoperative day and a return towards preoperative values by the fourth day after surgery. The increase in cough threshold on the first postoperative day correlated with the time since opiate administration (r = 0.7 for capsaicin, 0.52 for citric acid). These results show that the threshold concentration of chemical irritants causing cough is increased on the first postoperative day after upper abdominal surgery.
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PMID:Cough threshold after upper abdominal surgery. 233 May 54

The therapeutic inhibition of angiotensin converting enzyme (ACE) is associated with the production of a dry cough, which occurs more commonly in women than men and appears to be unrelated to concurrent illness. At present the exact incidence of ACE inhibitor cough and the substrate of ACE responsible for this effect is unknown. Cough challenge by inhalation of aerosols of tussive agents such as citric acid and capsaicin may be used to study the effect of drug administration on the cough reflex. In normal subjects, an oral dose of captopril (25 mg) causes a significant shift in the dose-response curve to capsaicin inhalation, but not that to distilled water or citric acid. The exacerbation of artificially induced cough by ACE inhibition may be the result of a local increase in perineuronal substance P or bradykinin concentrations within the lung.
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PMID:Cough associated with angiotensin converting enzyme inhibition. 247 6

In anaesthetized dogs exposed to SO2, nedocromil sodium prevented the increase in bronchial responsiveness to histamine challenge and suppressed the cellular changes taking place in the lung. In conscious dogs challenged with citric acid, by inhalation, nedocromil sodium prolonged the time to onset of coughing and had an inhibitory effect on the total number of coughs in each episode. Nedocromil sodium has been observed to stimulate bronchial C fibers, and it is suggested that this activity may relate to the antitussive effect of the compound.
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PMID:Effect of nedocromil sodium on SO2-induced airway hyperresponsiveness and citric acid-induced cough in dogs. 254 97


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