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)

1. Sulphated glycoprotein output from the trachea, isolated in situ, has been measured in anaesthetized cats by a radio-isotopic method. The effects of irritation of various parts of the airway on this mucus output were studied. 2. Mechanical stimulation of the nose and nasopharynx increased tracheal mucus output by reflexes which involved parasympathetic and probably also sympathetic motor pathways. 3. Laryngeal stimulation had a similar through the same motor pathways. 4. Inhalation of ammonia vapour into the lower airways reflexly increased mucus output from the isolated trachea. The efferent pathway for this reflex was mainly or entirely parasympathetic. It is argued that the afferent pathway involved cough receptors. 5. Lung inflation, inhalation of histamine aerosol and intravenous injection of phenyl diguanide (which excite mainly lung stretch receptors, lung 'irritant' receptors and alveolar 'J-receptors' respectively) had no consistent effect on tracheal mucus secretion. 6. The afferent and efferent pathways of these reflexes are discussed.
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PMID:The effects of irritation at various levels of the airway upon tracheal mucus secretion in the cat. 97 88

The effect of tramadol on laryngeal reflex activity was assessed in a double-blind cross-over study in six volunteers receiving single oral doses of either codeine 50 mg, tramadol 50 mg or tramadol 100 mg. Laryngeal reactivity was measured by the response to the inhalation of dilute ammonia vapour. The minimum ammonia concentration required to induce a glottic stop was recorded prior to drug administration, and at 15, 30, 45, 60, 90, 120, 150 and 180 min thereafter. Psychometric tests were performed at 0, 45 and 105 min to detect any relationship between central sedation and changes in laryngeal reflex activity. The concentration of ammonia required to induce a glottic stop increased in all treatment groups, but more so in the tramadol groups. The time course suggested that the codeine effect peaked early, and had returned to normal within 2 h. For tramadol 100 mg, laryngeal depression appeared to be still increasing at the end of the 3-h study period. No correlation was found between laryngeal and sedative effects. Tramadol is produced as a racemic mixture, in which one isomer acts through an opioid receptor pathway whilst the other affects noradrenergic and serotonergic mechanisms. Both of these routes of action may be involved in the suppression of the response to experimentally induced cough.
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PMID:A comparison of the effects of codeine and tramadol on laryngeal reactivity. 155 50

Respiration cycles through three distinct phases (inspiration, postinspiration, and expiration) each having corresponding medullary cells that are excited during one phase and inhibited during the other two. Laryngeal stimulation is known to induce apnea in newborn animals, but the cellular mechanisms underlying this effect are not known. Intracellular recording of ventral respiratory group neurons was accomplished in intact anesthetized, paralyzed, and mechanically ventilated piglets. Apnea was induced by insufflation of the larynx with ammonia-saturated air, smoke, or water. Laryngeal insufflation induced phrenic nerve apnea, stimulation of postinspiratory neurons, and stable membrane potentials in inspiratory and expiratory cells consistent with postinspiratory inhibition. Usually the membrane potential of each neuronal type cycled through an expiratory level before onset of the first recovery breath. Variants of the apnea response, probably reflecting the aspiration reflex or sniffing, sneezing, coughing, and swallowing, were also observed. These latter patterns showed oscillation between inspiration and postinspiration without an apparent intervening stage II expiratory phase. However, stage II expiratory activity always preceded onset of the first ramp inspiration after such a pattern. These findings suggest that activation of postinspiratory mechanisms causes profound alterations in the respiratory pattern and that stage II expiration importantly modulates recovery of ramp inspiratory activity. The mechanism of this latter effect may be inhibition of early inspiratory neurons with consequent postinhibitory rebound.
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PMID:Respiratory neuronal activity during apnea and other breathing patterns induced by laryngeal stimulation. 188 71

The authors followed up the health of 322 elementary-school pupils at Sabac who were exposed to increased air pollution with chemical agents (ammonia, fluor hydrogen, chloracetic acid, sulfur dioxide, soot). The mean annual concentration of these gases were above or insignificantly under maximally permitted values. The results of the examination were as follows: recurrent cough in 12.4 per cent of cases and clinical signs of chronic or obstructive bronchitis in 8.4 per cent of children. Values of vital capacity were under normal in 27.6 per cent of cases and almost in the half of children vital capacity was at the lower normal limit. FEV1/FVC was under normal in 15 per cent of cases and at the lower normal limit in about 18.6 per cent of children. In spite of a great number of children with positive cutaneous tests to inhalation allergens with Prick's method IgE was within normal limits in these children. Thus, a significant noxious effect of allergic components on respiratory organs should be excluded. This was also confirmed by spirometric measurements of the two subsequent maximal expiriums when differences of +/- 3% were registered. However, in children with allergic bronchitis the value dispersion was by 2-3 times greater. Consequently, the authors concluded that damaged respiratory organs in children at Sabac appeared in a greater number of cases than in other places and that these damages were due to increased concentrations of different chemical air pollution agents.
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PMID:[The status of the respiratory organs in students in Sabac exposed to increased air pollution]. 221 27

Monitoring of intracranial pressure (ICP) and efforts to keep the ICP below the critical level are vital in the treatment of Reye's syndrome. Continuous monitoring of ICP was carried out in 21 cases of Reye's syndrome who were at or beyond stage III at the time of admission to the Veterans General Hospital, between January 1981 and August 1986. Seventeen had ICP ranging from 15 mmHg to 67 mmHg. Three patients died, 1 in stage V with an ICP of 67 mmHg received a craniectomy, and 2 others were in stage IV with ICP's of 66 mmHg and 25 mmHg, respectively. The fatality rate was 14% (3/21). Among 18 patients, 5 had moderate psychomotor retardation (PMR), 4 had severe PMR and 2 had mild PMR. The remaining 7 patients survived without sequelae. Blood exchange transfusion could further reduce ICP and seemed to improve neurologic outcome. Blood ammonia higher than 400 micrograms% is indicative of a bad prognosis. Hyperventilation was the most rapid and effective means of reducing moderate degrees of increased ICP. During intensive supportive care, we also found that coughing, endotracheal intubation, seizures, asynchronous respiration to an artificial respirator, suction of the airway and any painful stimulation caused further increases in ICP and worsened the situation. Care should be given to avoid these factors.
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PMID:Continuous monitoring of intracranial pressure in Reye's syndrome--5 years experience. 228 26

In order to get a better knowledge on respiratory illnesses of children in Toulouse, and to evaluate the influence of air pollution, 1,000 children between 8 and 11 years of age, living in five different areas of the city were observed during one year (March 1985-March 1986), together with the measure of twenty pollutants. A questionnaire was used to assess the history of respiratory diseases and the chronic respiratory pathology. According to the areas, no difference appeared, other than the frequent cough which is more important in an area with lower social income (p less than 0.01). The acute respiratory illnesses, as noted during the year of observation, had a different pattern according to the areas (p less than 0.0001). Amongst the five pollutants used for the analytic study through the cross-correlations, four: nitrogen monoxide and dioxide, black fumes, and ammonia particulate derivatives are related to the respiratory diseases.
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PMID:[Respiratory symptoms in schoolchildren in Toulouse. Influence of atmospheric pollution]. 236 68

The influence of replacing the phenolic hydroxyl by the methoxy group on opioid receptor binding, analgesic and antitussive action was investigated in the corresponding couples morphine-codeine, hydromorphone-hydrocodone and O-desmethyltramadol (L 235)-tramadol. Binding was studied on rat whole brain membranes (without cerebellum) with the radioligands dihydromorphine (mu-site), ethylketocyclazocine (k-site), D-Ala2-D-Leu5-enkephalin (delta-site) and naloxone (no selective binding). Analgesia (tail flick) and antitussive action (NH3-vapour induced cough) was investigated in rats and ED50 values 10 min after i.v. application were calculated to compare efficacy. All free hydroxyl compounds had higher opioid receptor affinities than the corresponding methoxy derivatives and were more active at the mu-site. The methoxy derivatives codeine and tramadol only had low affinities lacking selectivity towards mu-, kappa-, or delta-binding. Hydrocodone in contrast showed strong and mu-selective binding. The hydroxy compounds had higher analgesic activity than the methoxy congeners and analgesia appeared to correlate with mu-binding affinity. Codeine and hydrocodone were weaker antitussives than the corresponding hydroxy compounds, whereas no significant difference was found between O-desmethyltramadol and tramadol. Only in the tramadol group the methoxy substitution increased antitussive potency in relation to analgesic potency.
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PMID:Receptor binding, analgesic and antitussive potency of tramadol and other selected opioids. 284 50

Twenty-one healthy and 21 asthmatic volunteers were exposed to respirable sulfuric acid aerosol (mass median particle diameter approximately 0.9 micron, geometric standard deviation 2.5) in a chamber at 21 degrees and 50% relative humidity. Measured sulfuric acid concentrations averaged 0, 380, 1060, and 1520 micrograms/m3 (in the occupational range, higher than concentrations observed in ambient air pollution). Exposures to different concentrations occurred in randomized order 1 week apart. They lasted 1 hr and included three 10-min periods of heavy exercise. Healthy volunteers showed no statistically significant changes in pulmonary function, airway reactivity to inhaled methacholine, or overall reporting of irritant symptoms which could be attributed to acid exposure. They did show a slight statistically significant (P less than .01) increase in cough with increasing acid concentration. At the two highest acid concentrations, asthmatics showed significant increases in irritant symptoms and decrements in pulmonary function, without significant changes in airway reactivity. Their function decrements appeared to increase with time during exposure. Previous studies in fog (10 degrees, median particle diameter approximately 10 micron) with similar concentrations of sulfuric acid showed more symptoms but less pulmonary function change, perhaps reflecting different sites of particle deposition in airways and/or different degrees of neutralization by airway ammonia. This and earlier evidence predicts little, if any, acute irritant response in short-term (1 hr or less) exposures to sulfuric acid at concentrations found in ambient air pollution.
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PMID:Respiratory dose-response study of normal and asthmatic volunteers exposed to sulfuric acid aerosol in the sub-micrometer size range. 305 19

Topically and intravenously administered local anaesthetic agents are widely used to inhibit cough, but little quantitative, pharmacological data seems to be available. Various aspects of local anaesthetic agents as inhibitors of cough and other airway reflexes are discussed. Nebulized lidocaine dose-dependently inhibited both mechanically (trachea, carina) and ammonia vapour-induced cough. Lidocaine had a similar potency on each type of cough but inhibited that caused by mechanical stimulation for a significantly longer period of time. This observation supports the hypothesis of a more peripheral location for receptors mediating chemical cough. Nebulized tetracaine appeared to be more potent and to have a significantly longer duration of action than lidocaine. The Hering-Breuer inflation reflex was attenuated by both agents and in doses larger than those needed to inhibit cough. This observation is compatible with the view that the cough receptors are located close to the airway lumen and those mediating the Hering-Breuer reflex within the smooth muscle. Airway anaesthesia is commonly used to block the cough reflex during endoscopic procedures. Nebulized lidocaine has been reported also to suppress severe chronic cough but further studies on airway anaesthesia and cough in acute and chronic lung disease are warranted.
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PMID:Airway anaesthesia and the cough reflex. 331 Dec 42

Vadocaine hydrochloride (2',4'-dimethyl-6'-methoxy-3-(2-methylpiperidyl) propionanilide hydrochloride, OR K-242-HCl; INN: vadocaine) is a novel antitussive compound structurally resembling local anaesthetics. Its antitussive profile was studied in several animal models. In guinea-pigs, vadocaine reduced by about 70% the cough episodes induced by sulphur dioxide or ammonia. The effective dose was 2.5 mg/kg p.o., and codeine phosphate was less effective. In cats, vadocaine (3 mg/kg i.v.) inhibited by about 80% for 10 min the cough reflex initiated by mechanical irritation of the trachea. When vadocaine was given via the vertebral artery, it was about 10 times more active than by the intravenous route. Codeine was 3 times as active as vadocaine by both routes. This result indicates an important central component in the antitussive action of vadocaine. In another cat model, 5 mg/kg of vadocaine was somewhat weaker than 1 mg/kg of codeine in inhibiting the cough caused by electrical stimulation of the laryngeal nerve (Domenjoz' method). In dogs, both oral and intravenous doses of 6 mg/kg of vadocaine and 2 mg/kg of codeine were approximately equiactive, inhibiting by 60-80% the cough induced by electrical stimulation of the trachea. Concentrations of vadocaine in serum were around 1 microgram/ml during oral administration. By both routes, the antitussive activity (inhibition of cough by 50% or more) lasted at least 2 h. Vadocaine caused local anaesthesia in the guinea-pig wheal preparation at concentrations of 0.25% and 0.5%, and on the guinea-pig cornea at 0.5%. Duration of anaesthesia was longer than that of lidocaine. Vadocaine did not affect the guinea-pig tracheal strip preparation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Antitussive action of the new anilide derivative vadocaine hydrochloride compared with codeine phosphate in four animal models. 339 94


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