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 early recognition and appropriate management of EIB can allow children and adolescents to fully participate in physical activities and sports. The diagnosis by history of chest congestion, coughing, and decreasing performance with exercise is helpful but is aided by a more systematic questionnaire that can detect otherwise "normal" people with EIB. The diagnosis is documented by performance of an exercise challenge test such as a treadmill or cycloergometer to verify bronchospasm induced by exercise. The management can be accomplished by nonpharmacologic means such as an early vigorous warmup, the use of a mask for rebreathing warmed air, and participation in a physical training program to increase anaerobic fitness. Pharmacologic management includes the appropriate use of cromolyn sodium, beta adrenergic agonists, theophylline, ipratroprium bromide, and calcium channel blocking agents. In addition the antihistamine, terfenadine, can also be utilized to effectively block exercise-induced bronchospasm. These pharmacologic agents can be utilized in both national and international competition when approved by the appropriate national governing body and/or the US Olympic Committee and the International Olympic Committee.
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PMID:Exercise-induced bronchospasm in clinical practice. 307 64

The effect of inhaled capsaicin, the irritant extract of pepper, on airway tone has been studied in humans. Inhaled capsaicin (2.4 X 10(-10) and 2.4 X 10(-9) mol) caused a dose-dependent fall in specific airways conductance (maximum fall 28 +/- 19 and 38 +/- 19%, respectively; means +/- SD, n = 17). This was maximal within 20 s of exposure and lasted for less than 60 s. There was no difference in the magnitude or duration of bronchoconstriction between normal, smoking, or asthmatic subjects. Capsaicin also caused coughing and retrosternal discomfort. On repeated exposure to capsaicin, there was no evidence for a reduced response (tachyphylaxis). Ipratropium bromide (0.25 mg by inhalation) significantly (P less than 0.05) reduced the bronchoconstriction (maximum falls 34 +/- 14 and 15 +/- 9% after saline and ipratropium bromide, respectively; means +/- SD n = 6), indicating that it was dependent on a cholinergic vagal reflex rather than on local release of substance P from nerves in the airway. Inhaled sodium cromoglycate (10 mg by nebulizer or 40 mg as a dry powder), however, had no significant effect on the bronchoconstrictor response. Capsaicin may be a useful tool for investigating nonmyelinated nerve reflexes in human airways.
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PMID:Bronchoconstrictor response to inhaled capsaicin in humans. 315 68

A 33-year-old female presented for elective excision of a posterior fossa tumour following two generalized seizures six months earlier. The patient had been asymptomatic on phenytoin 300 mg/day. Two h pre-operatively, a 300-mg dose of phenytoin was administered, general anesthesia induced and pancuronium bromide given to achieve neuro-muscular paralysis. Respiration was supported and anesthesia maintained with isoflurane and nitrous oxide in oxygen. Thirty min into the operation a further 2-mg dose of pancuronium bromide was administered. One h later, the patient coughed. A peripheral nerve stimulator was applied to the right common peroneal nerve with surface electrodes. Over the next 75 min a total of 15 mg of pancuronium bromide was required. With each dose there was a complete loss of response to peripheral nerve stimulation, followed by a rapid return of full train-of-four response, accompanied by coughing and cerebral engorgement. At this point, metocurine iodide was administered with full sustained paralysis for 45 min. Blood samples collected during a second operation indicated the patient had an extremely short pancuronium elimination half-life and a small volume of distribution. Several explanations are offered including phenytoin induction of hepatic microsomal enzymes responsible for the biotransformation of pancuronium, alterations in tissue or protein binding and/or alterations in myoneuronal junctional response.
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PMID:Pancuronium-phenytoin interaction: a case of decreased duration of neuromuscular blockade. 322 Jun 9

The pharmacologic treatment of cough can be divided into two main categories: therapy with controls, prevents or eliminates cough (i.e., antitussive) and therapy that makes cough more effective (i.e., pro-tussive). Definitive antitussive therapy depends on determining the aetiology or operant pathophysiologic mechanism and then initiating specific treatment; it can be almost uniformly successful. Non-specific antitussive therapy is directed at the symptom; it is indicated when definitive therapy cannot be given. For pathologic cough in man, predominantly studied in patients with chronic bronchitis, the following non-specific antitussive drugs have been shown to be effective: aerosolized ipratropium bromide, all narcotics of the phenanthrene alkaloid group (e.g., morphine and codeine), and the non-narcotics, dextromethorphan, glaucine, diphenhydramine, caramiphen, viminol and diviminol. Although studies have shown that hypertonic saline aerosol can improve cough clearance, there are no data, to date, that have convincingly demonstrated this agent or any other pro-tussive drug to be clinically useful.
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PMID:The effects of drugs on cough. 332 60

The effect of bradykinin was studied by inhalation in normal and asthmatic human subjects, as well as on human bronchial smooth muscle in vitro. Bradykinin caused cough and retrosternal discomfort in all subjects and bronchoconstriction in asthmatic subjects. Bradykinin was approximately 10 times more potent than histamine and methacholine, and there was a significant correlation between the subjects' sensitivity to histamine and bradykinin. Bradykinin-induced bronchoconstriction was prolonged when compared with that of histamine and the C-fiber stimulant capsaicin. This bronchoconstriction was subject to tachyphylaxis, which was also associated with desensitization of the subjects to inhaled histamine. The provocative dose causing a 35% fall in specific airway conductance (PD35) was unaffected by aspirin (1 g orally). However, ipratropium bromide (0.25 mg by nebulizer) significantly inhibited the effect of bradykinin, the PD35 being 0.8 mumol (range, 0.16 to 3.4) and 0.15 mumol (range, 0.047 to 1.15) after active dose and placebo, respectively (p less than 0.05). Likewise, cromolyn sodium (40 mg dry powder) also significantly reduced response to bradykinin, with a PD35 of 0.04 mumol (range, 0.13 to 0.31) after placebo and 0.39 mumol (range, 0.05 to 4.45) after SCG (p less than 0.05). Bradykinin only weakly constricted human bronchial smooth muscle in vitro. Bradykinin at 10(-4) caused only 21.5 +/- 5.5% of the maximal carbamylcholine contraction in 11 of 18 airways. Captopril did not enhance the effect of bradykinin. Bradykinin is a potent bronchoconstrictor of human airways in vivo, acting in part through cholinergic mechanisms but not because of the formation of prostaglandins.
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PMID:Bradykinin-induced bronchoconstriction in humans. Mode of action. 354 15

1. The antitussive properties of bronchodilators were evaluated in a total of 47 normal volunteers. 2. Cough was induced by inhalation of ultrasonically nebulized solutions of distilled water and hypotonic saline. 3. Inhaled fenoterol hydrobromide (360 micrograms; 20 volunteers) and inhaled ipratropium bromide (72 micrograms; 14 volunteers) both significantly reduced couch compared with placebo (P less than 0.01). Oral salbutamol sulphate (4 mg; 11 volunteers) and oral pirenzepine hydrochloride (50 mg; 14 volunteers) had lesser effects. 4. Cough inhibition correlated with a small but statistically significant degree of bronchodilatation as measured by specific airway conductance (sGaw) and forced expiratory volume in one second (FEV1) in six normal subjects studied with each treatment in a placebo controlled, double blind study (r = 0.67, P less than 0.001). 5. Small reductions in airway tone are associated with a reduced cough response elicited by inhaled ultrasonically nebulized distilled water.
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PMID:Inhibition of artificially induced cough in man by bronchodilators. 368 30

Long-term effects of ipratropium bromide (IB) were evaluated using a double-blind cross-over design in 23 adult chronic bronchitic participants. Two 20-micrograms doses of either IB or placebo were administered as an inhalant four times a day for a period of seven weeks. Sputum volume expectorated during a 24-hour period decreased significantly (p less than 0.05) over the entire length of the study, but sputum viscosity or its dry weight were not affected. Although total number of inflammatory cells in sputum was decreased by the use of IB (p less than 0.05), macrophages increased slightly. Subjects coughed less while receiving IB, and their cough was less severe (p less than 0.05). Ipratropium bromide caused a significant improvement (p less than 0.05) in the mechanics of breathing primarily in the subjects between 46 to 55 years of age. No major adverse reaction to IB was recorded.
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PMID:Sputum changes associated with the use of ipratropium bromide. 623 43

Ipratropium bromide (0.125 mg, 0.25 mg and 0.5 mg) and salbutamol (5 mg) by aerosolized solution produced equivalent peak bronchodilatation between one and two hours after administration to ten patients with chronic partially reversible airways obstruction. The duration of action of the two higher doses of ipratropium bromide (0.25 mg--6 hours; 0.5 mg--5 hours) was significantly greater than salbutamol (4 hours). FVC increases with both drugs and saline were greater than FEV1 increases which may indicate dilatation of small peripheral airways or removal of bronchial mucus from these sites after coughing. A dose of 0.25 mg ipratropium bromide as an aerosolised solution is recommended for clinical use.
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PMID:Comparison of ipratropium bromide and salbutamol by aerosolized solution. 645 76

To determine whether cough and bronchoconstriction result from alterations in the osmolarity or alterations in the ion concentration of inhaled aerosols and to determine if the specific ions in the aerosol are important, we had 9 subjects with mild asthma inhale various solutions while we recorded cough and measured specific airway resistance. To evaluate the effects of altering osmolarity and ion concentration separately, we administered aerosols of hypo-osmolar distilled water (0 mosm), iso-osmolar sodium chloride (308 mosm), iso-osmolar dextrose in water (308 mosm), hyperosmolar sodium chloride (1,232 mosm), and a hyperosmolar solution of dextrose and sodium chloride (1,232 mosm). To evaluate cough without bronchoconstriction, we had the subjects inhale metaproterenol before inhaling the same aerosols. To determine whether the absence of a specific ion was important in causing cough or bronchoconstriction, we had the subjects inhale iso-osmolar solutions of sodium bromide, sodium gluconate, and lysine monohydrochloride. We found that alteration in osmolarity away from iso-osmolarity of inhaled aerosols is a stimulus for bronchoconstriction in subjects with mild asthma. Absence of ions in the presence of iso-osmolarity is not a stimulus for bronchoconstriction, but the absence of a permeant anion is a stimulus for cough. Thus, we found that the responses of cough and bronchoconstriction to inhaled aerosols can be separated.
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PMID:Alteration in osmolarity of inhaled aerosols cause bronchoconstriction and cough, but absence of a permeant anion causes cough alone. 669 20

Although gastro-esophageal reflux (GER) is one of the major causes of chronic persistent cough (CPC) in the USA and in Europe, it is a rare cause of CPC in Japan. We report a rare case of CPC caused by GER, in which treatment with an H2-blocker or with a proton pump inhibitor was successful. A 65-year-old woman had complained of coughing for over 25 years. Her coughing was not alleviated by treatment with a bronchodilator (beta 2-adrenoceptor agonist), an anti-allergic agent, a corticosteroid, or a sedative. GER was considered as a possible cause of her coughing because exacerbation of the coughing was associated with the development of gastrointestinal symptoms (heartburn). Fiberoptic esophagoscopy showed esophagitis and esophageal herniation of the sliding type. Twenty four-hour monitoring of distal esophageal pH showed that the coughing occurred when the pH dropped below 4, and that the pH was less than 4 for about 7% of the whole monitoring time. An H2-blocker or a proton pump inhibitor completely eliminated the symptoms. Therefore, CPC caused by GER was diagnosed. We found that coughing could be induced by instillation of 0.1 N hydrochloric acid at the distal esophagus, and that the coughing was partially inhibited by inhalation of an anti-muscarinic agent (ipratropium bromide) and by esophageal instillation of 4% xylocaine. These data support the "reflex theory". Although CPC caused by GER is rare in Japan, we should remember that GER can be a cause of CPC even in Japanese patients.
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PMID:[A case of chronic persistent cough caused by gastro-esophageal reflux]. 766 22


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