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)

Differences between ventilatory response and metabolic rates of young rainbow trout tested within the sublethal range of pH 6 to pH 9 were observed using a flowing water respirometer. The oxygen consumption was monitored at swimming speeds of 12 cm/sec and 24 cm/sec. The oxygen consumption rates at 24 cm/sec and pH 6 (423 mg/kg-hr) and pH 9 (367 mg/kg-hr) were considerably higher than those determined near neutrality (328 mg/kg-hr). Ventilation rate increased to either side of neutrality, but significantly fewer respiratory reversals, or "coughs," were observed at pH 6 and a greater number at pH 9 than occurred at pH 7 and 8 or in untested fish. The respiratory-cough response is shown to be pH-dependent in rainbow trout and may therefore not be as reliable an indication of pollutant-caused stress in studies where the experimental pH has not been specified or controlled.
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PMID:Ventilation and metabolic rate of young rainbow trout (Salmo gairdneri) exposed to sublethal environmental pH. 0 17

The effect of the drug Ru 20201 (1,2,3,4,4a,9b-hexahydro,-8,9b-dimethyl-4-[3-(4-methylpiperazin-1-yl)propionamido]dibenzofuran-3-one upon mechanically-evoked cough from the laryngopharyngeal and tracheobronchial areas in nine unanaesthetized cats has been examined. Inhalation of 2 ml of an aerosol of a 10% solution in water suppressed coughing for 30 min. The effect was greatest on the number of cough efforts. The expiratory component of cough was suppressed more than was the inspiratory one. The effect was greater on cough from the laryngopharyngeal than from the tracheobronchial area.
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PMID:The antitussive actions of the drug Ru 20201 given as an aerosol to cats. 2 95

We studied waking and ventilatory responses to laryngeal stimulation during sleep in three dogs. The dogs breathed through an endotracheal tube inserted caudally into the trachea through a tracheostomy. Laryngeal stimulation was produced either by inflating a small balloon that was positioned in the rostral tracheal segment, or by squirting water onto the larynx through a catheter inserted through the tracheostomy. Airflow was measured with a pneumotachograph, and sleep state was determined by behavioral, electroencephalographic, and electromyographic criteria. We found that the degree of laryngeal stimulation required to produce arousal and coughing was higher in rapid-eye-movement (REM) sleep than in slow-wave sleep (SWS). Stimuli that failed to cause arousal from SWS often produced a single expiratory effort, or brief apnea (1--2 s) and bradycardia. In contrast, during REM sleep subarousal stimuli often resulted in prolonged apnea (greater than 10 s) and marked bradycardia. We conclude that during REM sleep arousal responses to laryngeal stimulation are depressed, but ventilatory and cardiac responses are intact.
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PMID:Waking and ventilatory responses to laryngeal stimulation in sleeping dogs. 21 83

We studied waking, ventilatory, and reflex tracheal smooth muscle (TSM) responses to tracheobronchial irritation or lung inflation in three sleeping dogs. The dogs breathed through a cuffed endotracheal tube, and airflow was measured with a pneumotachograph. TSM tone was monitored directly by measuring pressure in the water-filled cuff of the endotracheal tube. Mild degrees of tracheobronchia irritation, produced by squirting 0.1--1.0 ml of water into the lower trachea, or by having the dogs inhale one breath of acetic acid vapor (concentration 17 ppm), generally caused arousal from slow-wave sleep (SWS), but not from rapid-eye-movement (REM) sleep. During wakefulness the irritant stimuli caused coughing and TSM constriction; during SWS or REM sleep, these responses occurred only if the stimulus first produced arousal. In contrast, stimulation of pulmonary stretch receptors by lung inflation did not cause arousal, but readily produced apnea and TSM relaxation during SWS. The results indicate that cough and airway smooth muscle constriction in response to bronchopulmonary irritant stimuli do not occur in the absence of arousal, and that arousal responses to such stimuli are depressed in REM sleep.
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PMID:Arousal, ventilatory, and airway responses to bronchopulmonary stimulation in sleeping dogs. 22 19

The pathophysiology, symptoms and treatment of paraquat intoxication, primarily from oral ingestion, and the pharmacology and pharmacokinetics of paraquat are reviewed. Toxicity has occurred after topical application, oral ingestion or inhalation of paraquat. Systemic toxicity has not been reported from smoking of paraquat-contaminated marijuana but heavy abusers of contaminated marijuana may experience coughing, hemoptysis and mouth irritation. Following ingestion of 30 mg/kg or 50 ml of a 21% (w/w) solution of paraquat (as the base), hepatic, cardiac or renal failure or death may occur. Smaller doses (greater than or equal to 4 mg/kg of paraquat base) may cause respiratory distress, renal dysfunction or, occasionally, jaundice or adrenal cortical necrosis. When paraquat ingestion is suspected, the drug should be removed immediately from the gastrointestinal tract by gastric lavage or by whole-gut irrigation. Adsorbents such as Fuller's earth, bentonite or activated charcoal may be used during gastric lavage. Combined use of forced diuresis (with furosemide, mannitol and i.v. dextrose in water or normal saline), hemodialysis or hemoperfusion is recommended until the compound cannot be detected in body fluids or the dialysate. Immediate and effective treatment is necessary to prevent systemic toxicity or death from paraquat intoxication.
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PMID:Paraquat poisoning: a review. 36 Aug 33

The output of secretions from the airway submucosal glands is regulated by vagal efferent nerves. Stimulation of cough receptors increases mucus output reflexly via the vagus nerves. Adrenergic agonists increase submucosal gland secretions in some species, which indicates that adrenergic receptors are present in these cells. However, evidence for adrenergic nervous pathways to the glands is limited. Irritants and drugs stimulate secretion from epithelial cells by direct effects. There is also evidence that the secretion of epithelial cells can be stimulated by parasympathetic nervous pathways in birds but not in mammals. Active ion transport of Cl- toward the lumen and of Na+ toward the submucosa results in net ion movement toward the airway lumen in unstimulated tracheal epithelia. Drugs and mediators increase the net movement of ions toward the lumen. No agents have yet been found that increase net ion movement toward the submucosa. The link between ion transport and water secretion in airway epithelia, although speculative, seems likely in view of the evidence from other epithelia. Since airway epithelium is a "tight junction" epithelium, modification of the tight junction may alter the transepithelial movement of water and ions. We suggest that the depth and consistency of the periciliary layer of airway secretions determine the ability of the cilia to propel the mucoprotein gel and thereby modify mucociliary transport. To achieve this, secretion of mucus must be controlled separately from the secretion of water. Studies are needed to determine which of the specialized functions of the epithelial cells interact to regulate the clearance of secretions from the airway. Is the sol maintained by secretion and reabsorption of fluid across the epithelium? Does the sol move with the gel by ciliary action or does it remain stationary? Do changes in the epithelial tight junctions influence net water movement and thus indirectly alter the depth of the sol layer? To answer these questions, techniques are needed to study subunits of the airway, including isolated surface cells and submucosal glands; and sensitive methods are required to analyze the very small samples of secretions for glycoprotein and electrolyte content. Intracellular measurements of electrolyte concentrations and electrical potentials may help to elucidate the mechanisms of transepithelial ion and water movement. The control system for the production and removal of respiratory tract secretions may be altered in disease. For instance, chronic stimulation of cough receptors causes reflex secretion and may be the cause of the hyperplasia of submucosal glands and of the abnormal secretions that occur in chronic bronchitis and asthma (50, 58). The abnormally viscid mucus in cystic fibrosis may be due to a defect in Cl- transport, which provides too little water for both the gel and sol layers. These speculations are intended to identify areas for further research, which hopefully will reduce the morbidity and mortality in these common lung diseases.
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PMID:Control of mucus secretion and ion transport in airways. 37 97

Three cases of allergic alveolitis due to indoor humdification systems are described. Thermoactinomyces vulgaris precipitins were detected in the serum of a 37-year-old female patient who had typical febrile attacks during exposure to cool-mist from a home humidifier. When the cause was detected and eliminated, the symptoms and signs disappeared and the woman's gas transfer factor improved from 56% to normal within six months. In a printing office a 60-year-old woman had had febrile attacks with cough for more than a year. The patient herself associated the respiratory disease with a cool-mist humidifier sometimes used at work. The water reservoir was heavily contaminated with amoebas (Amoeba proteus), which might have been the causative organisms in this case. Aspergillus fumigatus precipitins were found in the serum of a 53-year-old female printer with the clinical picture of occupational allergic alveolitis. The same organism was detected in the ambient air of the printing office.
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PMID:Humidifier-associated extrinsic allergic alveolitis. 37 86

Airway reflexes are difficult to study in conscious animals because associated changes in ventilation alter intrathoracic airway dimensions. By studying an isolated segment of extrathoracic trachea, we have overcome this problem. In each of 2 dogs, we created surgically an isolated tracheal segment just below the larynx, sealed at one end and tapered at the other to a 3-mm opening via a skin fistula. A chronic tracheostomy was also created near the thoracic outlet. We monitored intraluminal pressure (Pseg) of the isolated segment to reflect changes in smooth muscle tone. During anesthesia, with pentobarbital, gentle mechanical stimulation of the carina, deflation of the lungs, and asphyxia for one min increased Pseg (+9 to +/- 16 cm H2O). Lung inflation and alveolar hyperventilation decreased Pseg (-9 to -16 cm H2O). Five breaths of 2 per cent histamine aerosol increased Pseg (+5 cm H2O) when resting tone was normal. We also coated lumen of the isolated segment with tantalum powder and documented roentgenologically changes in the size of the segment that reflected changes in smooth muscle tone; constriction and dilation in response to asphyxia and lung inflation, respectively, were demonstrated directly by this technique. In conscious dogs, lung inflation decreased Pseg, and carinal stimulation increased Pseg. Instillation of lidocaine hydrochloride (Xylocaine) into the isolated tracheal segment blocked cough caused by mechanical stimulation of the segment, but carinal stimulation still caused constriction of the segment under these conditions which indicated that afferent, but not effrent parasympathetic innervation of the segment had been blocked selectively. Conversely, instillation of atropine sulfate into the isolated tracheal segment blocked constriction of the segment caused by carinal stimulation, but mechanical stimulation of the segment still caused cough under these conditions, which indicated that efferent, but not afferent parasympathetic innervation of the segment had been blocked selectively. We conclude that an innervated extrathoracic tracheal segment constricts and dilates via cholinergic pathways and is suitable for the study of airway reflexes in conscious dogs.
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PMID:A chronic isolated tracheal segment to study airway reflexes in conscious dogs. 46 75

Pseudoephedrine hydrochloride (I), brompheniramine maleate (II), and dextromethorphan hydrobromide (III) in a cough-cold sytup were separated and determined by ion-pair reversed-phase high-pressure liquid chromatography. The separation was carried out using a muBondapak C18 column (30 cm x 3.9 mm i.d.) and a mobile phase of acetonitrile-water-acetic acid (40:60:1) with 0.01 N 1-octanesulfonic acid sodium salt and 0.05 N potassium nitrate. Detection was accomplished using a UV detector at 265 nm for I and II; III was monitored at 280 nm. Concentration versus peak height plots in the ranges of 0.37-1.9 mg/ml for I, 0.025-0.126 mg/ml for II, and 0.125-0.625 mg/ml for III were linear. Ten consecutive injections of a mixture gave a percent relative standard deviation of less than 1% for all three components. Average recoveries from laboratory-prepared samples were 100.5% for I, 100.9% for II, and 100.1% for III. No precolumn cleanup was necessary, and the chromatogram was complete in 16 min.
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PMID:Ion-pair reversed-phase high-pressure liquid chromatography of cough-cold syrups I: pseudoephedrine hydrochloride, brompheniramine maleate, and dextromethorphan hydrobromide. 51 4

Progressively severe sneezing, rhinorrhea, cough, wheezing, and dyspnea developed in a spray-painter, apparently in relation to exposure to a particular spray paint. A monitoring of exposure at work revealed the development of symptoms and a decrease in peak flow rates. Subsequent challenges in the laboratory performed under conditions resembling occupational exposure resulted in dual asthmatic responses on exposure to the whole paint (98 per cent methyl methacrylate emulsion and 2 per cent dimethyl ethanolamine solution) and to dimethyl ethanolamine solution (2 per cent) alone. Water, methyl methacrylate emulsion, and 1,4 dioxane (0.6 per cent) used as a thinner in the dimethyl ethanolamine did not produce a response in the airways. Allergy skin tests with dimethyl ethanolamine and a mixture of dimethyl ethanolamine and human serum albumin were negative. To our knowledge, this is the first report of asthma and/or rhinitis induced specifically by dimethyl ethanolamine. The mechanism of the specific reactivity is not known.
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PMID:Dimethyl ethanolamine-induced asthma. 85 20


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