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Query: UMLS:C0010200 (cough)
 23,843 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Larynx resistance changes have been studied in the dog by means of in situ isolated glottis technique. Bronchiolar tone changed through isoprenaline and histamine administration, and after recurrent and vagus nerve bilateral section. Isoprenaline administration (0.1 mg/kg) was followed by larynx resistance decrease, expiratory duration increase, and expiratory abdominal pressure decrease with regard to respiration preceded by rest. Cough response by mechanical tracheal stimulation and glottis closing by larynx stimulation were abolished after isoprenaline administration. Histamine administration (0.1 mg/kg) was followed by larynx resistance increase, expiratory duration decrease, expiratory abdominal pressure increase, and expiratory abdominal pressure/maximum expiratory airflow relation increase. Larynx resistance decreased after recurrent nerve bilateral section, and increased later when vagus nerves were sectioned.
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PMID:[Bronchopulmonary influences in larynx resistance (author's transl)]. 74 Oct 70

The manner in which a cigarette is smoked varies considerably between individuals and may be an important determinant of the altered bronchial reactivity observed in cigarette smokers. Twenty smokers were examined to determine the relationship between cigarette smoke inhalation patterns and bronchial reactivity. Inhalation patterns were measured non-invasively with a respiratory inductive plethysmograph and these were related to the provocative concentration of histamine that caused a 20% fall in FEV1 (PC20) and to the cough threshold for inhaled citric acid. Histamine PC20 values were inversely correlated with depth and rate of inhalation. Cough threshold was inversely correlated with greater cigarette consumption and with depth of inhalation.
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PMID:Cigarette smoke inhalation patterns and bronchial reactivity. 335 77

Bronchial hyperreactivity was studied in 79 patients who gave a history of allergic symptoms. Twenty-nine of them suffered from rhinitis, 28 from eczema, 21 from urticaria and one from gastrointestinal allergy. Forced expiration in the first second (FEV1) was measured in each. If FEV1 was greater than 1 l a histamine challenge was done. Histamine (0.6 mg/ml) was inhaled by tidal breathing for one minute. FEV1 was measured before the inhalation and two min after cessation of the inhalation. If FEV1 dropped greater than 20% the inhalation was assessed as positive and the provocation was stopped. If the challenge was not positive another inhalation with histamine (2.4 mg/ml, l min) was done. If FEV1 dropped greater than 20% when measured two min after the inhalation the provocation was called positive. Twenty-two patients with rhinitis had a negative bronchial challenge, six had a positive. One of them had asthma, three suffered also from cough and/or serous sputum production, and two had hay fever. Out of 28 with eczema, 20 had negative histamine challenge and five a positive. Four of these suffered from daily cough and/or serous sputum production, one had no airway symptoms. Fifteen out of 21 suffering from urticaria had a negative histamine challenge, three had a positive. Two of them suffered from asthma and one complained of daily cough and/or serous sputum production. It is concluded that allergic subjects without symptoms from the airways, have a bronchial reactivity to inhaled histamine similar to the general population.
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PMID:Bronchial hyperreactivity in allergic subjects. 346 10

As part of a study of the morphology of hyperreactive airways, 22 heavy smokers (67 +/- 31 pack-years), all male, were challenged with histamine, questioned on symptoms and skin-tested for common allergens before thoracic surgery, mainly for cancer. Histamine was delivered with a hand operated nebulizer in a total dose of 7.8 mumol or a 20% fall from the baseline FEV1. The PD20 (dose of histamine which causes a 20% fall of FEV1) was determined on a semi-log dose-response curve. Symptoms were recorded by physician-administered questionnaire and skin tests were performed with 8 common allergens. Values for FEV1%VC ratio and response to salbutamol were taken from preoperative spirometric studies. Bronchial hyperresponsiveness (BHR) was found in 45% of the patients. The PD20 was in the range of asthma. Past symptoms of airway allergy did not enhance BHR risk. Half of the 13 subjects with airway obstruction (FEV1%VC of less than 2 SD of the predicted value) had normal bronchial responsiveness; however, PD20 correlated well with FEV1 (% predicted) in the hyperresponsive group (r = 0.90, p less than 0.001). The degree of BHR was unrelated to tobacco consumption, number of positive skin tests and response to salbutamol. Symptoms were those of chronic bronchitis and bronchoconstriction (wheezing, morning chest tightness, sudden dyspnea), as well as cough. They were experienced, to some extent, by 82% of patients, only half of whom had BHR. These smokers with BHR differed from asthmatics in that half of them did not report bronchoconstriction symptoms and none experienced chest discomfort during provocation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Relation between respiratory function, bronchial reactivity and symptoms in heavy smokers]. 376 98

The tussive and bronchoconstrictive effects of histamine inhalation in 7 normals, 7 asthmatics, and 24 patients with chronic cough (PCC) were measured by counting coughs during a standard histamine inhalation challenge. All PCC had a tussive response. Fifteen PCC exhibited significant linear correlations between cough count and either the change in forced expiratory volume at 1.0 (delta FEV1) or conductance-volume ratio (sGaw) (delta sGaw). Normals and asthmatics had little or no cough. Metaproterenol pretreatment in seven PCC reduced both the FEV1 and cough response to histamine without changing the relationship between cough and delta FEV1. The tussive and bronchoconstrictive effects of methacholine inhalation were also measured in 7 asthmatics and 16 PCC. One asthmatic coughed. Fifteen PCC coughed. There were significant linear correlations between cough count and delta FEV1 or delta sGaw in 10 PCC. At comparable delta FEV1 and delta sGaw, histamine produced more cough than methacholine. These data indicate that during inhalation of histamine or methacholine by PCC cough is related to, and may be caused by, bronchoconstriction. Histamine also causes cough by an additional mechanism not related to bronchoconstriction.
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PMID:Comparison of the tussive effects of histamine and methacholine in humans. 635 79

The pharmacological mechanisms of allergic cough in the guinea pig were studied. Actively sensitized guinea pigs were exposed to aerosols of antigen to elicit coughing. In separate experiments, naive guinea pigs were exposed to aerosols of capsaicin to elicit coughing. Both allergic and capsaicin-induced cough were inhibited by loratadine (0.3-10 mg kg-1 p.o.) and chlorpheniramine (0.1-3.0 mg kg-1 p.o.). Neither cimetidine (10 mg kg-1 s.c.), nor thioperamide (3-10 mg kg-1 s.c.), inhibited allergic or capsaicin-induced cough. Codeine (3-30 mg kg-1 p.o.), salbutamol (0.003-3.0 mg kg-1 s.c.) and ipratropium (0.03-1.0 mg kg-1 s.c.) inhibited both allergic and capsaicin-induced cough. Hexamethonium (10 and 30 mg kg-1 s.c.) inhibited allergic, but not capsaicin-induced cough. Allergic and capsaicin-induced cough were unaffected by phenidone (5.0 and 10.0 mg kg-1 s.c.). Indomethacin (5.0 and 10.0 mg kg-1 s.c.) had no effect on allergic cough but slightly inhibited capsaicin-induced cough. We conclude that allergic and capsaicin-induced cough are modulated by histamine H1 receptor and cholinergic mechanisms. Histamine H2 or histamine H3 receptor mechanisms, and lipoxygenase and cyclooxygenase products of arachidonic acid metabolism do not influence allergic and capsaicin-induced cough. Ganglionic mechanisms play a minor role in the production of allergic cough and no role in capsaicin-induced cough.
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PMID:Pharmacological studies of allergic cough in the guinea pig. 749 4

1. Capsaicin, prostaglandin E2 (PGE2) and histamine are potent stimuli for reflex coughing and bronchoconstriction in many species including man. We have studied the effects of solutions of capsaicin, PGE2 and histamine on airway sensory receptors when administered as inhaled aerosols to the lower respiratory tract in anaesthetized, paralysed and artificially ventilated cats. 2. Histamine, administered by aerosol (6 breaths of a 1 mg ml-1 solution) and intravenously (10 micrograms kg-1), caused an increase in the rate of discharge from rapidly adapting stretch receptors (RARs) and caused bronchoconstriction. 3. Six breaths of a capsaicin aerosol generated from solutions of 0.1 or 1 mg ml-1 stimulated six out of nine RARs tested. Bronchoconstriction occurred with and without RAR stimulation. The diluent for the capsaicin aerosol had no significant effect on pulmonary mechanics or rate of RAR discharge. 4. Administration of increasing concentrations (0.001-1 mg ml-1) of PGE2 aerosol given in six breaths (at 6 min intervals) caused a dose-dependent increase in the rate of discharge of eight RARs tested and caused bronchoconstriction. The diluent for the PGE2 aerosol had no effect on pulmonary mechanics or rate of RAR discharge. 5. Inhalation of aerosols of histamine (6 breaths of 1 mg ml-1 solution) and capsaicin (3 breaths of 0.1 mg ml-1 solution) stimulated all six lung C fibre endings studied (3 pulmonary and 3 bronchial). These aerosols of capsaicin and histamine also caused bronchoconstriction. 6. We conclude that solutions of capsaicin and PGE2, when delivered by aerosol to the airway epithelial surface, are not selective stimulants of C fibres. Both agents can stimulate RARs. Activation of some but not all RARs tested, by inhaled capsaicin, suggests that there are subpopulations of capsaicin-sensitive and -insensitive receptors. Stimulation of airway RARs by a range of pharmacologically active agents released by airway inflammation may contribute to reflex coughing and bronchoconstriction in man.
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PMID:Effects of aerosol-applied capsaicin, histamine and prostaglandin E2 on airway sensory receptors of anaesthetized cats. 827 Dec 11

1. Increased histamine concentrations are found in the plasma and urine following allergen challenge in allergic subjects. This study compared a controlled challenge with clinically relevant doses of inhaled and injected histamine, as indicative of an allergic response, in an attempt to validate the use of urinary histamine or 1-methylhistamine measurements as an objective, non-invasive diagnostic test. 2. Inhalation of histamine produced peripheral vasodilation, increased heart rate, a fall in partial expiratory flow rate (pEFR) and blood pressure, 'tight chest' and cough. Subcutaneous injection produced vasodilation and headache but no change in heart rate or blood pressure. 3. Plasma histamine concentrations were similar in the two studies. Inhalation of increasing doses of histamine through a nebuliser (output 0.13 ml min-1) resulted in an increase from a mean of 0.30 to 1.65 ng ml-1, with return towards baseline within 20 min. Injection of 1 mg histamine s.c. produced an increase from 0.32 to 1.4 ng ml-1 within 5 min, remaining above 1 ng ml-1 for 30 min. 4. There was a significant increase of 15.2 ng mg-1 creatinine in urinary histamine concentration following the injection of histamine (P = 0.04) and an increase of 11.4 ng mg-1 creatinine when histamine was given by inhalation (P = 0.18). Histamine excretion rate increased by 108 ng min-1 (P = 0.04) after inhalation and by 37.2 ng min-1 (P = 0.09) after injection. Urinary 1-methylhistamine concentrations were significantly raised following both histamine inhalation (+ 238 ng mg-1 creatinine; P = 0.013) and injection (+ 180 ng mg-1 creatinine; P = 0.03).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Plasma concentrations and urinary excretion of histamine after inhalation and subcutaneous injection of histamine. 844 35

A 38-year-old woman with a history of seasonal rhinoconjunctivitis reported repeated attacks of wheezing after drinking various alcoholic beverages. Two consecutive histamine provocations using two identical samples of red wine containing 200 micrograms histamine/l and 3,700 micrograms/l, respectively, were performed in a double-blind placebo-controlled fashion to assess a possible histamine-induced bronchoconstriction. Lung function, plasma histamine, skin temperature, pulse rate and symptoms were assessed. In 3 male controls, four consecutive wine tests were performed in a randomised double-blind placebo-controlled fashion. Drinking wine with 3,700 micrograms histamine/l caused coughing and wheezing with a decrease in lung function. Plasma histamine showed an increase at 10 and 20 min and decreased at 30 min both after histamine-rich as well as histamine-poor wine, reaching the peak increase after histamine-rich wine. Controls did not react and plasma histamine levels did not increase. Bronchoconstriction after wine or food rich in histamine seems to be caused by diminished histamine degradation on the basis of reduced activity of diamine oxidase. Histamine in wine may induce bronchoconstriction in patients suffering from histamine intolerance.
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PMID:Histamine in wine. Bronchoconstriction after a double-blind placebo-controlled red wine provocation test. 876 8

Desloratadine (descarboethoxyloratadine, CAS 100643-71-8) is an active metabolite of loratadine (CAS 79794-75-5) that exhibits qualitatively similar pharmacodynamic activity with a relative oral potency in animals 2.5-4 times greater than loratadine. Its antihistaminic effect lasts 24 h. Desloratadine was shown to be a selective H1 antagonist with more potent antihistaminic activity in vitro than either loratadine or terfenadine (CAS 50679-08-8), as indicated by its displacement of 3H-mepyramine from H1 receptors in rat brain, guinea pig brain, and guinea pig lung, and by its antagonism of histamine-induced contractions of guinea pig ileum. Antihistaminic activity and anitallergic effects also were observed in vivo. After oral administration, desloratadine was 2.5 to 4 times more potent than loratadine in protecting against histamine-induced lethality in the guinea pig and paw edema in the mouse; after topical administration, it was almost 10 times more potent in antagonizing histamine-induced increases in nasal microvascular permeability in the guinea pig. Histamine-induced changes in pulmonary resistance and compliance were also prevented by oral administration of desloratadine and loratadine in the monkey. An oral antiallergic effect was demonstrated by important reductions of acute bronchospasm in the allergic monkey and potent inhibition of allergic cough in the guinea pig. These preclinical studies provide evidence that desloratadine is an antihistaminic agent with a greater potency than loratadine and, together with results from numerous published studies, suggest an antiallergic effect of desloratadine.
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PMID:Preclinical pharmacology of desloratadine, a selective and nonsedating histamine H1 receptor antagonist. 1st communication: receptor selectivity, antihistaminic activity, and antiallergenic effects. 1080 Jun 33


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