methylatropine and Asthma

Topics: Airway Resistance; Albuterol; Animals; Asthma; Atropine; Atropine Derivatives; Bronchi; Carbachol; Dose-Response Relationship, Drug; Histamine; Humans; In Vitro Techniques; Methacholine Chloride; Methacholine Compounds; Muscle Contraction; Muscle, Smooth; Serotonin; Trachea

Topics: Adrenergic beta-Agonists; Asthma; Atropine; Atropine Derivatives; Bronchi; Bronchial Provocation Tests; Bronchitis; Drug Combinations; Humans; Ipratropium; Mucus; Parasympatholytics; Respiratory System

The bronchodilator effect of nebulized AMN, albuterol and their combination was evaluated in 16 steroid-dependent asthmatic children. In phase 1, maximal bronchodilation was determined by dose-response studies on separate days. Maximal bronchodilator dose of each drug was administered either alone or in combination during phase 2. In phase 1, 0.11 +/- 0.01 mg/kg of albuterol and 0.03 mg/kg of AMN produced maximum bronchodilation. In phase 2, the peak response to albuterol occurred within 30 min and to AMN, at 60 min. Maximal FEV1 achieved after AMN was 90 percent of the maximal achieved after albuterol. AMN FEV1 response was better than for placebo for 3 h; that for albuterol was better for 4 h. Combination therapy produced a peak response similar to that of albuterol but was better than albuterol by 6 h. Thus, the maximum bronchodilator effect of AMN is less than that of albuterol in asthmatic children, but the combination may extend the period of bronchodilatation.

Topics: Adolescent; Albuterol; Asthma; Atropine Derivatives; Bronchi; Child; Double-Blind Method; Drug Therapy, Combination; Female; Humans; Male; Parasympatholytics; Pulmonary Ventilation; Randomized Controlled Trials as Topic

The combination of nebulized atropine methylnitrate (AMN) and a beta-agonist has been shown to produce greater and longer lasting bronchodilation than either drug alone. We examined the efficacy of the combination in diminishing the "morning dipping" in PEFR in eight hospitalized but stable asthmatics. The patients received nebulized albuterol along with either AMN (AMN + ALB) or placebo (ALB) in a random double-blind cross-over fashion at 10 PM on four nights. PEFR and FEV1 were recorded at 6 PM, 10 PM, and 6 AM before the administration of bronchodilators. There was no statistically significant difference between ALB and AMN + ALB in reducing the morning dipping in these patients.

Topics: Administration, Inhalation; Adolescent; Adult; Albuterol; Asthma; Atropine Derivatives; Bronchodilator Agents; Child; Circadian Rhythm; Double-Blind Method; Drug Therapy, Combination; Female; Forced Expiratory Volume; Humans; Male; Nebulizers and Vaporizers; Peak Expiratory Flow Rate

This is a double-blind, placebo-controlled crossover study designed to assess the effectiveness of nebulized atropine methylnitrate (AMN) with chronic use. We studied 22 patients with asthma, 10 receiving theophylline and inhaled beta-agonists and 12 who were receiving corticosteroids as well. All had demonstrated at least a 15% change in FEV1 either spontaneously or after bronchodilator. Bronchodilator effect was measured serially for 4 h after inhalation of the initial dose and again after 2 wk of four-times-daily use. Significant bronchodilator effect was seen initially with AMN when compared to placebo (p less than 0.01). After 2 wk of use, the bronchodilator effect of AMN was significantly diminished as compared to the initial effect (p less than 0.01) but was still better than placebo (p less than 0.05). Subsensitivity did develop to varying degrees in the patients, but we were unable to identify any clinical parameters that would allow prediction of subsequent subsensitivity. We conclude that the development of subsensitivity to AMN occurs in certain patients with chronic administration but does not reflect a total loss of bronchodilator effect.

Topics: Adult; Aged; Asthma; Atropine Derivatives; Bronchodilator Agents; Clinical Trials as Topic; Double-Blind Method; Drug Tolerance; Forced Expiratory Volume; Humans; Middle Aged; Random Allocation

In ten adult patients with severe, partially reversible airflow obstruction due to asthma, with or without co-existent chronic bronchitis, the acute bronchodilator responses of ipratropium bromide (40 micrograms) and terbutaline (500 micrograms) from metered-dose inhalers, atropine methonitrate (2 mg) as a wet aerosol and placebo were compared in a double blind trial. Also the combination of ipratropium bromide and terbutaline aerosols was compared with both ipratropium and terbutaline alone in short-term and long-term studies. In the short-term study, all the drugs produced significant bronchodilatation compared with placebo. The responses to ipratropium bromide and terbutaline alone were not significantly different. The combination of ipratropium bromide with terbutaline did not produce significantly greater changes in the FEV1, SGaw or static lung volume than terbutaline alone. Atropine methonitrate however, produced significantly greater changes of the airway conductance (SGaw) and static lung volumes (TLC and RV) but not FEV1, when compared to ipratropium bromide. When administered over randomised periods of one month each there were no significant differences between the combination of ipratropium bromide and terbutaline and each drug alone in daily airflometer recordings, daily symptom scores or fortnightly spirometry and clinical assessment. It is concluded that ipratropium bromide, in the conventional dose of 40 microgramm by metered-dose inhaler produces safe, effective bronchodilatation. Its effect, however, did not significantly augment that of the beta adrenergic stimulant, terbutaline and was less than that of atropine methonitrate 2 mg by wet aerosol.

Topics: Aerosols; Aged; Airway Obstruction; Asthma; Atropine Derivatives; Clinical Trials as Topic; Double-Blind Method; Drug Combinations; Humans; Ipratropium; Male; Middle Aged; Random Allocation; Terbutaline

Topics: Administration, Intranasal; Aerosols; Aged; Asthma; Atropine Derivatives; Clinical Trials as Topic; Dose-Response Relationship, Drug; Double-Blind Method; Drug Therapy, Combination; Fenoterol; Humans; Male; Middle Aged; Random Allocation

In order to delineate the clinical profiles which correspond to different patterns of responsiveness to inhaled anticholinergic drugs (i.e. atropine methonitrate, ipratropium bromide), 102 subjects tested with these drugs and with beta 2-adrenergic bronchodilators were classified into three groups, namely: a group with positive skin prick tests (group 1), a group with blood or sputum eosinophilia but negative skin prick tests (group 2), and a group with negative skin prick tests and neither blood nor sputum eosinophilia (group 3). All had reversible airflow obstruction and their clinical profiles closely corresponded to atopic asthma, non-atopic asthma and chronic bronchitis, respectively, but the prevalence of mucus hypersecretion was similar in all three groups. Pharmacologically, group 1 patients were distinguished from the other two groups by their significant impairment of 1-second forced expiratory volume response to the bronchodilator action of anticholinergic drugs. This is the physiological correlate of atopic asthma.

Topics: Adult; Aged; Airway Resistance; Albuterol; Asthma; Atropine Derivatives; Bronchitis; Female; Forced Expiratory Volume; Humans; Ipratropium; Isoproterenol; Lung Diseases, Obstructive; Male; Middle Aged; Parasympatholytics; Respiratory Hypersensitivity

85 subjects with 20% reversibility in FEV1 were classified into the categories of asthma (55 patients) and non-specific airflow obstruction (30 patients), respectively, on the basis of the presence or absence of eosinophilia (in the blood or sputum). Asthmatics were further subdivided into the atopic and non-atopic subgroups, respectively, on the basis of skin prick tests. Clinically, paroxysmal nocturnal wheezing was more significantly associated with asthma than with non-specific airflow obstruction. Atopic asthmatics were distinguished from patients with non-specific airflow obstruction by their younger age at presentation and at onset of obstructive symptoms, by a history of allergic provocation of wheezing, a family history of asthma and other atopic diseases, and by a lower incidence of mucus hypersecretion. The last 3 symptoms also distinguished atopic from non-atopic asthma. Furthermore, unlike patients with non-atopic asthma or patients with non-specific airflow obstruction, atopic asthmatics had a significant impairment of bronchodilator responsiveness to inhaled anticholinergic drugs.

Topics: Adolescent; Adult; Aged; Airway Resistance; Albuterol; Asthma; Atropine Derivatives; Bronchial Provocation Tests; Eosinophilia; Female; Forced Expiratory Volume; Humans; Intradermal Tests; Ipratropium; Isoproterenol; Lung Diseases, Obstructive; Male; Middle Aged; Parasympatholytics; Respiratory Hypersensitivity

Responsiveness to anticholinergic bronchodilators was assessed in 19 atopic and in 36 non-atopic asthmatics of comparable mean age and basal FEV1. Atopic subjects had a significantly lower degree of responsiveness (p less than 0.01). When the 19 atopic subjects were matched for FEV1 and age with 19 non-atopic subjects (selected from the group of 36) the difference in responsiveness to anticholinergic drugs was still evident (p less than 0.01). Atopic status thus appears to have a significant effect on bronchial reactivity to inhaled anticholinergic drugs.

Topics: Adult; Aged; Albuterol; Asthma; Atropine; Atropine Derivatives; Female; Humans; Hypersensitivity, Immediate; Ipratropium; Male; Middle Aged; Skin Tests

We have examined the inhibitory effect of atropine and sodium cromoglycate (SCG) on the bronchial response to sulphur dioxide (SO2) in groups of normal and asthmatic subjects. Eleven normal subjects were premedicated with propranolol (100 mg orally) one hour before each experiment. After baseline measurements of specific airways conductance (sGaw) the subject inhaled an aerosol from a Wright nebuliser for five minutes. In separate experiments this contained water (control), atropine methonitrate (0 . 2%), or SCG (1%). Fifteen minutes later sGaw was remeasured and the subject then breathed SO2 (8 ppm) for three minutes through the mouth. Specific airways conductance was measured for the duration of the subsequent response. Intervals between experiments on any one subject were one week or more. After control SO2 inhalation sGaw decreased in all subjects (mean 34 +/- 17 (SD)%). Atropine and SCG significantly inhibited the SO2 response (p less than 0 . 01 for both). After atropine the mean decrease in sGaw was 13 +/- 24%; after SCG 16 +/- 12% (range -3- + 55%). With atropine the degree of inhibition was inversely related to the subject's responsiveness to the control SO2 inhalation (r = 0 . 75; p less than 0 . 01). In four asthmatics (without beta-blockade and with lower SO2 exposure) atropine did not inhibit the SO2 response; SCG had a similar effect to that seen in normal subjects. Therefore, vagal efferent mechanisms are involved in the bronchial response to SO2 in normal subjects, but the lack of inhibition caused by atropine in hyperreactive normal and asthmatic subjects suggests that vagal mechanisms are not important in the causation of hyperreactivity to SO2. The mechanism of inhibition with SCG is unknown.

Topics: Adult; Aerosols; Airway Resistance; Asthma; Atropine Derivatives; Bronchi; Bronchial Provocation Tests; Constriction, Pathologic; Cromolyn Sodium; Humans; Middle Aged; Premedication; Propranolol; Sulfur Dioxide; Time Factors

Topics: Adrenergic Agents; Asthma; Atropine; Atropine Derivatives; Biomedical Research; Epinephrine; Humans; Isoproterenol; Respiratory Function Tests; Respiratory Therapy; Toxicology

Topics: Asthma; Atropine; Atropine Derivatives; Humans; Isoproterenol