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. The effect of breathing an anaesthetic aerosol of 5% bupivacaine hydrochloride has been assessed in dog and man. 2. In the dog, the cough reflex was abolished and the Hering-Breuer inflation reflex severely impaired or abolished; breathing became slower and deeper; no pathological changes were found in the lungs of these dogs. 3. In man, no untoward effects resulted from a 10 min period of aerosol inhalation; there were no systematic effects on airway resistance or lung volumes and the cough reflex in response to either tactile or chemical (citric acid aerosol) stimulation was invariably abolished. The Hering-Breuer inflation reflex was impaired, but this was not associated with any change in resting ventilation. The Ve/CO2 response was enhanced after aerosol anaesthesia; subjects felt an exaggerated dyspnoea. The aerosol anaesthesia abolished the afferent pathway of a reflexly elicited bronchoconstriction in one subject. There was no effect on the ability to hold the breath, or on the quality of the associated sensation. 4. Control aerosols of sodium chloride solution or phosphate buffer produced no effects. Control experiments with intravenous infusions of bupivacaine proved that none of the effects could have been produced by systemic effects of the absorbed anaesthetic. 5. Plasma concentrations of bupivacaine in man did not exceed a recognized toxic level. The experiments demonstrate a safe reversible anaesthesia of the airways in man lasting for a period of 10-20 min.
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PMID:The effect of anaesthesia of the airway in dog and man: a study of respiratory reflexes, sensations and lung mechanics. 127 53

The effect of inhaled prostaglandin (PG) F2 alpha on the response to the inhaled tussive agent capsaicin was investigated in normal subjects. Seven subjects inhaled three breaths of four doses of capsaicin (0.3, 0.6, 1.2, and 2.4 nmol) before and immediately after inhaling PGF2 alpha (0.1 mumol) or placebo (0.15M NaCl) on separate days. The numbers of capsaicin induced coughs were greater after PGF2 alpha (mean 42.3 coughs) than after 0.15M sodium chloride (30.1). Visual analogue scores (0-10 on a 10 cm continuous scale) showed that capsaicin was more irritant after PGF2 alpha than after saline. Total respiratory resistance (Rrs), measured by the forced oscillation technique, was unaltered throughout the study. A double blind, placebo controlled study of the effects of inhaled salbutamol (200 micrograms, 0.6 mumol) and ipratropium bromide (40 micrograms, 0.1 mumol) on cough induced by capsaicin (2.4 nmol) and by PGF2 alpha (0.1 mumol) and on PGF2 alpha augmented, capsaicin induced coughing was performed in seven subjects. Neither drug had any effect on capsaicin induced coughing. Salbutamol reduced coughing due to PGF2 alpha (mean 7.7 coughs after salbutamol, 9.3 after placebo) but ipratropium bromide did not (mean 6.9 coughs after ipratropium bromide, 6.6 after placebo). Salbutamol also inhibited the augmentation of the capsaicin induced cough that followed inhalation of PGF2 alpha (mean augmentation 1.9 coughs after salbutamol, 4.1 after placebo), whereas ipratropium bromide did not (augmentation 1.7 coughs after ipratropium bromide, 2.7 after placebo). No changes in Rrs were seen after PGF2 alpha or either drug. Thus salbutamol reduces PGF2 alpha induced cough and the augmentation of capsaicin induced cough that follows PGF2 alpha.
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PMID:Prostaglandin F2 alpha enhancement of capsaicin induced cough in man: modulation by beta 2 adrenergic and anticholinergic drugs. 214 56

1. The ventilatory response to maximal incremental exercise and the accompanying sensation of breathlessness were studied after the inhalation of 0.9% sodium chloride (saline) and 5% bupivacaine aerosols in six patients with interstitial lung disease. 2. The adequacy of airway anaesthesia induced by bupivacaine aerosol was confirmed by the absence of the cough reflex to 5% citric acid aerosol on completion of exercise. 3. All subjects first performed a trial exercise test to familiarize them with the procedure and to assess the degree of arterial oxygen desaturation on exercise. In subsequent tests, supplementary oxygen was given to maintain the saturation at 95% or above. 4. Airway anaesthesia had no effect on the ability to perform exercise as assessed by maximum workload, CO2 production or heart rate. No significant changes were seen on the pattern of breathing, minute ventilation or end-tidal PCO2 on exercise. There was, however, a small but statistically significant increase in ventilation related to CO2 production (VE/VCO2) at the end of exercise. 5. There was a tendency for breathlessness to be increased by airway anaesthesia but this did not reach statistical significance. 6. These results provide no evidence that vagal afferent activity is responsible for the abnormal ventilatory response to exercise in patients with interstitial lung disease. The perception of breathlessness in these patients was not diminished by anaesthesia of the airway.
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PMID:Ventilation and breathlessness on maximal exercise in patients with interstitial lung disease after local anaesthetic aerosol inhalation. 334 36

In a group of patients with mild asthma the inhalation of mist derived from ultrasonically nebulised distilled water caused an increase in cough and a fall in FEV1. Double blind administration for five minutes of sodium cromoglycate (from an original solution containing 30 mg/ml) or atropine (2 mg/ml) by inhalation from a Minineb nebuliser, 30 minutes before the mist challenge, caused a significant reduction in the fall in FEV1 (p less than 0.05), but not in cough, by comparison with the protection afforded by placebo (saline). In a second study the fall in FEV1 caused by the inhalation of distilled water was not significantly different from that seen in response to hypotonic sodium chloride (1.7 g/l, 58 mmol/l), but both produced a significantly greater fall than did a similar mist containing sodium cromoglycate at an original concentration of 10 mg/ml (58 mmol/l). The results show that both atropine and sodium cromoglycate can block the fall in FEV1 due to mist and that protection by sodium cromoglycate is immediate. These results suggest that sodium cromoglycate blocks the nervous reflexes concerned in the response to mist, probably in the afferent limb of the reflex.
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PMID:Sodium cromoglycate and atropine block the fall in FEV1 but not the cough induced by hypotonic mist. 643 1

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

The effects of pretreatment with lignocaine administered intravenously on the insertion of the laryngeal mask airway were investigated in 80 unpremedicated, ASA 1 or 2, adult day-case patients in a randomised, double-blind, placebo-controlled trial. Patients received either intravenous lignocaine 1.5 mg.kg-1 or an equivalent volume of sodium chloride 0.9%. Induction of anaesthesia was achieved with propofol given via a syringe driver at a fixed rate of 600 ml.h-1 until the patient dropped a weighted syringe. No opioid or sedative drugs were given prior to induction. Pain on injection of propofol was recorded. Jaw opening, ease of insertion of the laryngeal mask, coughing, gagging and airway patency were all scored on three-point scales immediately after mask insertion re-attempted. This cycle was continued until success was achieved and the number of such cycles recorded. There were no differences between the lignocaine and control groups with respect to induction dose of propofol, degree of jaw opening, or amount of gagging. Laryngeal mask insertion was facilitated by pretreatment with lignocaine administered intravenously, without an alteration in induction dose of propofol (p < 0.05). Coughing and airway obstruction were both significantly reduced by pretreatment with lignocaine, as was the incidence of failure of insertion requiring deepening of anaesthesia (p < 0.05).
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PMID:Facilitation of laryngeal mask insertion. Effects of lignocaine given intravenously before induction with propofol. 748 6

To assess the effects on bronchial responsiveness of nebulized glutathione (GSH), one of the most efficient scavengers of oxidant substances in the airways, we studied eight patients with mild asthma (FEV1, 88 +/- 11% predicted [SD]) in a randomized, double-blind, cross-over, placebo-controlled fashion. Bronchial challenge was measured using both FEV1 and total pulmonary resistance (Rrs) by the forced oscillation technique. Patients received nebulized GSH (600 mg with 4 ml of 0.9% sodium chloride) or placebo (identical saline solution) over a period of 25 min, 1 wk apart. Placebo provoked subclinical mild bronchoconstriction (changes from baseline: FEV1, -1%; Rrs, +17%); by contrast, GSH caused major airway narrowing (changes from baseline: FEV1, -19%; Rrs, +61%) and induced cough (four patients) or breathlessness (three patients). Differences between placebo and GSH after challenge were also noticeable in both FEV1 (p = 0.03) and Rrs (p = 0.02). Neither osmolarity (660 mosm.kg-1) nor pH (3.0) of the GSH solution accounted for these effects. Nebulized salbutamol (5.0 mg) given before the GSH challenge blocked GSH-induced bronchoconstriction. Furthermore, GSH-induced FEV1 falls were inversely correlated with metabisulfite bronchoprovocation (provocative dose [PD20], 1.49 +/- 1.83 mumol) but not with methacholine challenge. The detrimental effects of nebulized GSH on the airway bronchial tone in patients with mild asthma strongly suggests bronchoconstriction provoked by sulfite formation.
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PMID:Nebulized glutathione induces bronchoconstriction in patients with mild asthma. 927 19

Ninety patients were assigned randomly in a double-blind manner to receive 0.9% sodium chloride, mivacurium 0.04 mg.kg-1 or mivacurium 0.08 mg.kg-1 intravenously, followed by propofol 2.5 mg.kg-1. A laryngeal mask airway (LMA) was inserted 90 s later. The LMA was positioned correctly during the first attempt in 87% of patients and this was not significantly altered by the use of mivacurium. However, mivacurium decreased the incidence of swallowing, coughing, movement and laryngospasm (p < 0.05). LMA insertion was graded as easy in 88% of patients who had mivacurium, compared with 50% in patients who had propofol alone (p < 0.05). The conditions during LMA insertion were similar after 0.04 or 0.08 mg.kg-1 of mivacurium. Patients were apnoeic for a mean (SD) time of 0.67 (0.72) min after propofol alone, compared with 1.72 (1.06) min and 3.05 (1.36) min in patients who also received mivacurium 0.04 and 0.08 mg.kg-1, respectively (p < 0.01). Patients who received mivacurium had a lower incidence of postoperative sore throat (24-30% vs. 53%) (p < 0.05). In conclusion, low-dose mivacurium facilitates LMA insertion and decreases the incidence of postoperative sore throat.
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PMID:The use of low-dose mivacurium to facilitate insertion of the laryngeal mask airway. 965 25

Eighty-six adult day-case patients were recruited into a prospective, randomised study and allocated to one of two groups. Patients received either intravenous remifentanil 0.3 microg.kg(-1) or an equivalent volume of sodium chloride 0.9% followed by induction of anaesthesia with propofol target-controlled infusion until the effect (brain) site calculated concentration was 2 microg.ml(-1). Jaw opening and ease of laryngeal mask insertion were assessed immediately after mask insertion. A higher incidence of failure of induction of anaesthesia was observed in the control group compared with the remifentanil group [15 (35%) vs. 3 (7%); p < 0.01] and addition of remifentanil significantly increased the ease and success of laryngeal mask insertion, with grade 1 (no coughing/gagging) conditions observed in 29 (68%) of the remifentanil group and 21 (49%) of the control group (p < 0.01). The doses of remifentanil and propofol used were not associated with any significant cardiorespiratory instability. In conclusion, when combined with propofol target-controlled infusion, remifentanil 0.3 microg.kg(-1) facilitates laryngeal mask insertion with minimal adverse haemodynamic changes.
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PMID:Facilitation of laryngeal mask airway insertion: effects of remifentanil administered before induction with target-controlled propofol infusion. 1153 80

The child who presents with acute coma runs a high risk of cardiopulmonary insufficiency, direct brain injury or even cerebral herniation. The case-management of such child requires a coma-specific emergent evaluation, immediate treatment of any hypoxicischemic insults and of the underlying cause. The coma-specific examination includes performance of child-adapted Glasgow Coma Score, the evaluation of brain stem functions such as pupillary response to light, cough- and gag reflex, and determination of all vital signs including body temperature. Treatment of hypoxicischemic insults includes control of airways and ventilation in patient with coma defined as GCS <8; liberal treatment of impaired cardiovascular states with isotonic fluids such as 0.9% sodium chloride; and treatment of cerebral herniation with head elevation, mannitol, hypertonic sodium chlorid fluids, steroids and hyperventilation. Immediately treatable causes are hypoglycemia, meningitis/encephalitis, opioid overdose and status epilepticus. Exclusion of rapidly progressive intracranial lesions almost always requires referral to the tertiary centre with head CT-scan facilities. Finally, an extensive etiology search of the stable coma is performed by looking for disease or trauma of the brain, for metabolic causes, for intoxications and for cardiopulmonary problems.
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PMID:[The comatose child]. 1613 15


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