Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The non-specific bronchial reactivity and cough threshold of hypertensive patients on an ACE-I monotherapy regimen (either captopril or enalapril), a beta 1-antagonist monotherapy regimen (either atenolol or metoprolol) or a combination of an ACE-I with a beta 1-antagonist were determined in the present study. Forty-six hypertensives who were on these medications performed a histamine inhalation test (to assess bronchial reactivity) and a further 36 of these individuals participated in the citric acid test (to assess cough threshold). A control cohort consisting of 25 age-matched, drug-free subjects also performed the citric acid test. The incidence of bronchial hyperreactivity was not significantly different between the ACE-I monotherapy regimen and the beta 1-antagonist monotherapy regimen (Chi-squared = 0.248). However, when the monotherapy regimens were pooled and compared with the ACE-I and beta 1-antagonist combination regimen, the combination regimen was found to be associated with a significantly higher incidence of bronchial hyperreactivity (Chi-squared = 6.69). No difference was observed between the age-matched controls and the hypertensive patients in terms of their cough threshold.
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PMID:The effect of angiotensin converting enzyme inhibitors (ACE-I) and selective beta 1-antagonists on bronchial reactivity and the cough reflex in man. 257 76

Prostaglandins may cause hyperresponsiveness to bronchoconstrictor agents in the lung and hyperalgesia in the skin. Increased airway concentration of both prostaglandins and bradykinin has been suggested as the possible cause of the increased cough sensitivity sometimes found in patients with cough associated with taking drugs that inhibit angiotensin-converting enzyme. We have therefore investigated the effect of prostaglandin E2 (PGE2), bradykinin (BK), histamine (H), and citric acid (C) on capsaicin-induced cough and increase in respiratory resistance (Rrs). Capsaicin-induced changes in Rrs and dose-cough response were measured before and after inhaling 0.76 mumol of PGE2, BK, H, and C. All the test substances caused cough, which was subject to tachyphylaxis, but no significant change in Rrs. Neither BK, H, nor C altered the capsaicin cough or Rrs response. However, PGE2 significantly increased both responses to capsaicin, the geometric mean (95% Cl) for the dose of capsaicin causing 5 or more coughs being 16.2 (14.3 to 18.3) nmol before and 4.4 (2.4 to 7.9) nmol after PGE2 (p less than 0.05). The percent increase (95% Cl) in Rrs after capsaicin was 20 (16.5 to 23.5)% before and 37.2 (32.2 to 43.2)% after PGE2 (p less than 0.05). The results suggest that the cough reflex will be increased in the presence of PGE2 in the airway.
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PMID:Sensitivity of the human cough reflex: effect of inflammatory mediators prostaglandin E2, bradykinin, and histamine. 275 Nov 60

1. The effects of nedocromil sodium, sodium cromoglycate and codeine phosphate on citric acid-induced cough have been studied in conscious tracheostomised dogs. 2. Nedocromil sodium (approximately 15 mg given as an aerosol) and codeine phosphate (5 mg kg-1, i.v.) significantly increased the time to the first cough when dogs were challenged with citric acid aerosol. The mean number of coughs in the initial period of coughing fell after treatment of dogs with nedocromil sodium or with codeine phosphate, but this reduction in mean cough number was not statistically significant. 3. Neither sodium cromoglycate (approximately 15 mg given as an aerosol) nor saline had significant effect on a citric acid challenge. 4. It is concluded that nedocromil sodium, but not sodium cromoglycate, possesses an anti-tussive action that may result from inhibition of sensory nerve activity in the lung. Nedocromil sodium may prove useful in the treatment of unproductive cough in situations where the use of a centrally-acting antitussive is undesirable.
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PMID:The effect of nedocromil sodium, sodium cromoglycate and codeine phosphate on citric acid-induced cough in dogs. 283 11

The effect of inhibition of angiotensin-converting enzyme (ACE) on standard cough challenge was investigated in a double-blind, randomised study in sixteen normal volunteers. Captopril (25 mg) or matched placebo was given by mouth 2 h before inhalation of nebulised distilled water, citric acid, and incremental doses of capsaicin (0.5-20 mumol/l). Distilled water and citric acid challenge were not significantly changed by captopril pretreatment. However, captopril significantly shifted the dose-response curve to capsaicin inhalation. The geometric mean dose of capsaicin causing 20 coughs/min was 1.3 mumol/l for captopril and 2.8 mumol/l for placebo pretreatment (p = 0.04). Cough is a recognised side-effect of ACE inhibitors; the observation that cough challenge is changed by these drugs in normal subjects implies a role for ACE in the cough reflex, possibly by metabolism of substrates other than angiotensin I.
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PMID:Angiotensin-converting enzyme and the cough reflex. 289 21

Coughing was induced in seven normal and eight asthmatic subjects by giving successive inhalations of citric acid aerosols of progressively higher concentration (range 0.5-32%). A baseline cough response was obtained on each of four experimental days, and there was no significant difference between days in this respect. Then the subjects received by inhalation either a bronchodilator (salbutamol 5 mg or ipratropium 1 mg) or placebo, in a paired double blind crossover design. A second citric acid run followed and was used for paired drug-placebo comparisons. In the asthmatic subjects the cough response was diminished by both bronchodilators (p less than 0.05), and the cough threshold was significantly higher after ipratropium but not salbutamol. In normal subjects no significant effects were found. Airways calibre was assessed, by an oscillatory technique that measures the resistance of the respiratory system (Siemens Siregnost FD 5), in four of the seven normal and all eight asthmatic subjects. The mean respiratory resistance was higher in asthmatic than in normal subjects, and fell significantly after both bronchodilators. In normal subjects smaller decreases in respiratory resistance occurred, significant only with salbutamol. The simplest hypothesis which explains the results relates change in cough response to altered neuroreceptor sensitivity associated with rapid changes in bronchial calibre.
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PMID:Effect of bronchodilators on the cough response to inhaled citric acid in normal and asthmatic subjects. 293 14

Neural pathways involved in cough and reflex bronchoconstriction and the effects of drugs on these airway reflexes have been studied in unanaesthetised guinea-pigs exposed to aerosols of citric acid (0.13-0.78 M), capsaicin (30 microM), nicotine (9.2 mM) and histamine (0.9 mM). The number of coughs was counted during the first 3 min of exposure and the time to onset of signs of dyspnea, as an indication of bronchoconstriction, was measured. Citric acid produced bronchoconstriction and dose-dependently increased the number of coughs. Capsaicin produced both cough and bronchoconstriction. Nicotine mainly produced cough and histamine bronchoconstriction. Pretreatment of adult guinea-pigs with capsaicin (50 mg kg-1 s.c.) produced a long-lasting (greater than or equal to 10 weeks) depletion of substance P- and calcitonin gene related peptide-like immunoreactivities in the sensory nerves of the larynx, tracheobronchial tree and lung. In capsaicin-treated animals, citric acid (0.39 M) and capsaicin (30 microM) caused neither cough nor bronchoconstriction. Nicotine (9.2 mM) and mechanical stimulation still produced cough, and histamine (0.9 mM) bronchoconstriction. It is concluded that in guinea-pigs both capsaicin-sensitive (probably C-fibre endings) and capsaicin-resistant (probably rapidly adapting stretch receptors) afferent neurons may be involved in cough and reflex bronchoconstriction.
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PMID:Cough and bronchoconstriction mediated by capsaicin-sensitive sensory neurons in the guinea-pig. 298 Feb 86

Twenty two normal women volunteers underwent a standard cough provocation test by inhaling solutions of citric acid of progressively increasing concentration. Eight were non-smokers, eight moderate smokers, and six occasional smokers. All the non-smokers and moderate smokers coughed. Moderate smokers tended to cough more than non-smokers, but not significantly so. None of the occasional smokers coughed at all (p less than 0.001). Possibly the ability to smoke occasionally with enjoyment is a marker for a diminished cough reflex.
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PMID:Cough response to citric acid aerosol in occasional smokers. 309 42

Antitussive activity of the new antitussive drug, levodropropizine (S(-)-3-(4-phenyl-piperazin-1-yl)-propane-1,2-diol, DF 526), was evaluated in healthy volunteers by the classical method of citric acid-induced coughing. Levodropropizine dose-dependently reduced cough frequency. Maximal inhibition was observed at 6 h after administration. Cough intensity was also reduced, as shown by the analysis of cough noise. Levodropropizine, at the dosage of 60 mg t.i.d., had no adverse effects on respiratory function nor on airway clearance mechanisms: in fact, it did not affect spirometric parameters. Levodropropizine had no effects on the rheological properties of mucus nor on ciliary activity of airway epithelium.
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PMID:Antitussive activity and respiratory system effects of levodropropizine in man. 319 11

The cough reflex has been investigated in insulin dependent diabetic patients with and without autonomic neuropathy. The cough response to inhaled citric acid was determined in eight patients with diabetes who had severe autonomic neuropathy and compared with that in 10 who had no evidence of neuropathy. The patients with autonomic neuropathy had a higher median threshold for the cough response to citric acid (median 50%, range 20- greater than 100%) than non-neuropathic control patients (median 10%, range 2-20%). These results suggest that vagal innervation of the bronchial tree is damaged by diabetic autonomic neuropathy.
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PMID:Cough threshold to citric acid in diabetic patients with and without autonomic neuropathy. 321 54

A plethysmographic method was employed to assess the airway resistance of conscious, free-breathing guinea-pigs. Using this method animals sensitized by inhalation of ovalbumin and appropriate controls were assessed for their responsiveness to histamine and methacholine in vivo. The cough frequency on exposure to citric acid mist in the two groups was also assessed. Tracheal spirals from these animals were subsequently tested for their responsiveness to histamine, methacholine and prostaglandin D2 in vitro. Sensitization increased responsiveness to histamine, methacholine and citric acid in vivo but only histamine responses were affected in vitro. These changes were accompanied by a significant eosinophilia in the airways as assessed by bronchoalveolar lavage. We conclude that sensitization of the airways to ovalbumin results in responsiveness changes in bronchial smooth muscle accompanied by signs of airway inflammation.
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PMID:Active sensitization of guinea-pig airways in vivo enhances in vivo and in vitro responsiveness. 322 83


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