human
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Eight patients with exercise-induced asthma participated in a single-blind trial comparing the protective effects of inhaled lignocaine ( estimated dose 48 mg ) , sodium cromoglycate ( estimated dose 12 mg ) , and ipratropium bromide ( estimated dose 120 μg ) . Saline was used as control . Effects were assessed from the mean maximal percentage fall in forced expiratory volume in one second ( FEV1 ) and maximal mid-expiratory flow rates ( MMFR ) after they had run on a treadmill for eight minutes . There was no significant change in baseline FEV1 or MMFR before each agent was given . Saline , lignocaine , and sodium cromoglycate did not alter the mean baseline FEV1 or MMFR significantly .  Ipratropium  caused bronchodilatation with an increase of 16·3 % in the mean FEV1 ( p<0·001 ) and of 43·4 % in the mean MMFR ( p<0·05 ) . After exercise the maximal percentage falls in FEV1 ( means and SEM ) after saline , lignocaine , sodium cromoglycate , and ipratropium bromide were 38·1 % ( 5·0 ) , 34·5 % ( 6·1 ) , 11·3 % ( 3·7 ) , and 19·3 % ( 7·4 ) respectively . Similarly , the mean maximal falls in MMFR  after saline , lignocaine , sodium cromoglycate , and ipratropium bromide were 54·4 % ( 5·2 ) , 52·9 % ( 7·7 ) , 23·6 % ( 6·6 ) , and 32·1 % ( 10·5 ) respectively . The inhibitory  effects of sodium cromoglycate and ipratropium bromide were significant whereas lignocaine failed to produce an effect . These results suggest that mediator release is an important factor in exercise-induced asthma and that in some patients the effects of the mediators may be on the postsynaptic muscarinic receptors . Local anaesthesia of sensory vagal receptors , on the other h and , does not prevent exercise asthma and these receptors do not appear to have any important role in exercise-induced bronchoconstriction The effects of ipratropium bromide ( 80 and 200 micrograms ) and placebo on the basal bronchial tone and on methacholine-induced bronchoconstriction were investigated in 10 asthmatic patients in a placebo-controlled double-blind manner . Bronchial hyperreactivity to methacholine was confirmed at a pretrial bronchial challenge . The patients were r and omly allocated to two groups in which the drug was inhaled from either metered-dose inhalers ( MDI ) or powder capsules . With the high dosage , the bronchodilation result ing from powder capsules was somewhat more pronounced than that achieved with the MDI . Otherwise the bronchodilator effect of ipratropium bromide and the protection afforded by the drug against methacholine-induced bronchoconstriction were similar in the two groups . In five patients the bronchodilator effect was better and in four patients the tolerance to methacholine was greater after the higher ipratropium dosage than after the lower one . In two patients ipratropium bromide had no bronchodilator effect but gave good protection against methacholine-induced bronchoconstriction . It is concluded that some patients benefit from a dosage of ipratropium bromide higher than that usually recommended and that an anticholinergic effect on the bronchi is possible even in the absence of the bronchodilator effect in the basal state BACKGROUND In acute asthma the optimal duration of treatment with combination β agonist and anticholinergic nebuliser solutions is unknown ; most studies have investigated single doses or treatment for up to 12 hours . To determine whether longer treatment with ipratropium bromide might aid recovery a study was undertaken in 106 patients with acute asthma . METHODS A double blind , r and omised , placebo controlled , three group study was performed with all patients receiving ipratropium for 12 hours and salbutamol for 60 hours after admission ( both nebulised four hourly ) , systemic steroids and , if necessary , theophylline . At 12 hours ipratropium was stopped in group I ( n = 35 ) but was continued in the other two groups , and at 36 hours ipratropium was also stopped in group II ( n = 35 ) while patients in group III ( n = 36 ) continued with ipratropium for 60 hours . Spirometric tests were performed before and after salbutamol , and again 30 and 60 minutes after ipratropium or placebo at 12 , 36 and 60 hours . Peak flow rates ( PEFR ) were measured before and after each nebulisation . RESULTS There were no differences between the groups in PEFR on admission ( group I : 214 l/min , group II : 198 l/min , group III : 221 l/min ) , or mean forced expiratory volume in one second ( FEV1 ) at 12 hours ( group I : 1.8 l , group II : 2.0 l , group III : 2.2 l ) , 36 hours ( group I : 2.1 l , group II : 2.3 l , group III : 2.4 l ) , or at 60 hours ( group I : 2.2 l , group II : 2.3 l , group III 2.5 l ) . Despite this , median time to discharge was significantly higher for patients in group I ( 5.4 days ) than for those in groups II ( 4.1 days ) and III ( 4.0 days ) . CONCLUSIONS Combination nebulised therapy can be continued beyond 12 hours and up to 36 hours after admission with improved recovery time . Lung function testing may not reflect the full benefit of treatment In order to determine the duration of action of the inhaled anticholinergic agent oxitropium bromide , a controlled study of the effect of pre-treatment with oxitropium bromide 200 micrograms against cholinergic challenge was carried out in ten asthmatic subjects ( 6 children , 4 adults ) . After baseline measurements of lung function ( FEV1 and sGaw ) and methacholine PC20 ( the concentration of methacholine to produce a 20 % fall in FEV1 ) oxitropium bromide or placebo were inhaled double-blind on 2 separate days . Lung function and methacholine PC20 were then measured at 1 , 3 and 6 h post dosing . Oxitropium bromide caused significant protection from methacholine challenge for 6 h ( p less than 0.05 ) A multi-center , double-blind , 90-day study compared an ipratropium bromide metered-dose inhaler ( 40 microgram four times a day ) with a metaproterenol metered-dose inhaler ( 1,500 micrograms four times a day ) in 164 patients with asthma ; of the 144 patients who completed the study , 71 received ipratropium and 73 received metaproterenol . Our results suggest that both drugs were equally effective bronchodilators . Although the shape of the pulmonary function response curves suggested that ipratropium has different bronchodilator kinetics than metaproterenol ( in that it has a slower onset of action and a more prolonged duration ) , comparison of the areas under the curves for the two drugs showed that there was no statistical difference between ipratropium or metaproterenol . The only significant side effects noted with ipratropium were cough and exacerbation of symptoms ; no anticholinergic side effects were noted Forty-nine asymptomatic asthmatic children who showed exercise induced bronchospasm ( EIB ) , received in a r and omized double-blind fashion one of the four following drugs administered through nebulizer and facial mask : salbutamol 4 mg ( 13 patients ) , disodium chromoglycate 20 mg ( 12 patients ) , ipratroprium bromide 0.4 mg ( 12 patients ) , placebo ( 12 patients ) . They performed exercise fifteen minutes after receiving the drugs and spirometries were done 0 , 5 , 10 , 15 and 20 minutes after the end of the exercise . Bronchodilation was noticed 15 minutes after the administration of salbutamol and ipratroprium bromide but not after cromoglycate or placebo . No patient receiving either salbutamol or cromoglycate had EIB whereas it occurred in 50 % of those receiving ipratroprium bromide and 91.6 % of those receiving placebo Thirty seven children with acute asthma were given nebulised ipratropium or placebo 30 minutes after their first dose of salbutamol and eight hourly thereafter . There were no significant differences between the two groups in clinical scores , peak expiratory flow rates , length of stay in hospital , or the need for oral steroids Six asthmatic children were studied to determine whether supplemental , parenteral atropine would increase the effects of bronchodilation and protection against exercise-induced bronchoconstriction after maximal effects had been achieved by inhalation . First , we determined the amount of inhaled atropine sulfate that would give maximal bronchodilation for each patient at rest . This quantity of atropine was design ated as " A. " Then all subjects exercised for five sessions with the following pre-exercise treatments in a r and om order : ( a ) inhaled distilled water plus intramuscular ( IM ) saline solution ; ( b ) inhaled A dose of atropine plus IM saline solution ; ( c ) inhaled distilled water plus 0.35 mg IM atropine ; ( d ) inhaled A dose of atropine plus 0.35 mg IM atropine ; and ( e ) inhaled double the A dose plus IM saline solution . The results showed that the combination of inhaled and IM atropine had the greatest bronchodilation effect and the greatest protection against exercise-induced bronchoconstriction .  Atropine inhalation alone ( A dose ) or IM injection ( 0.35 mg ) was not as effective in bronchodilation or in alleviation of exercise-induced bronchoconstriction . Doubling the dose of inhalation ( 2A ) did not increase the effects of the A dose . These results support the hypothesis that inhaled atropine does not reach all the airways where cholinergic receptors are present Until now very few studies have been performed on the prevention of exercise-induced asthma ( EIA ) in children with ipratropium bromide + fenoterol .  This is why we decided to study 30 children aged between 6 and 15 years , whose EIA was confirmed by a test including a 6-min free race on day 1 of the study . The criterion was a decrease of more than 20 % of the basal values of forced expiratory volume in 1 s ( FEV1 ) or FMF .  Children whose FEV1 or FMF baseline values were under 60 % of those expected according to Polgard tables were excluded . Three tests were performed , the first to determine EIA , the second was performed 72 h later after inhalation of placebo . 72 h after day 2 the patients returned in order to repeat the test , but this time , aerosol therapy with the combination ipratropium + fenoterol was applied prior to the race . The dosage of the combination was 1 puff of aerosol per 10 kg body weight , up to a maximum of 4 puffs . Each puff of the combination contains 0.02 mg of ipratropium bromide and 0.05 mg fenoterol . Functional assessment of children was carried out by means of forced spirometry . There were no significant differences between the placebo group and the group which received no medication , but there was a significant difference between the treated group and the other two , not only in the FEV1 and FMF values but also in forced vital capacity TEST . ( ABSTRACT TRUNCATED AT 250 WORDS A number of drugs are known to inhibit exercise-induced asthma ( EIA ) , but the results in some cases have been difficult to interpret due to the techniques employed . A comparative study was carried out in a group of children to investigate the effects of  salbutamol , choline theophyllinate , cromolyn sodium , atropine , and placebo . The exercise test took the form of six minutes of st and ardized treadmill running . All the drugs , but not the placebo , were able to inhibit EIA ti a significant degree , the effect being most marked with salbutamol . Cromolyn sodium caused no bronchodilatation at rest , while all the other drugs were brondhocilators , the effect being most marked with the atropine during exercise . It was impossible to distinguish the type of drug used for inhibition of EIA if it caused bronchodilatation at rest . The manner in which an exercise test can be used to investigate the duration of action or site of action of drugs is noted Glycopyrrolate , a quaternary ammonium anticholinergic compound is a potentially useful bronchodilator . To determine the efficacy , optimal dose , and duration of action of inhaled glycopyrrolate , we gave the drug to 11 asthmatic patients . Each subject received placebo or glycopyrrolate ( 100 , 200 , 600 , or 1,200 micrograms ) by inhalation in a double-blind , r and omized , crossover design . Measurements included FEV1 , FVC , heart rate , and blood pressure before administration of the drug and periodically for 12 hours . For eight hours following all doses of glycopyrrolate , both FEV1 and FVC ( both as percent of predicted ) were significantly greater for drug than for placebo . Glycopyrrolate may be a useful long-acting drug for the treatment of asthma 
    Output:
    
agent
***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Eight patients with exercise-induced asthma participated in a single-blind trial comparing the protective effects of inhaled lignocaine ( estimated dose 48 mg ) , sodium cromoglycate ( estimated dose 12 mg ) , and ipratropium bromide ( estimated dose 120 μg ) . Saline was used as control . Effects were assessed from the mean maximal percentage fall in forced expiratory volume in one second ( FEV1 ) and maximal mid-expiratory flow rates ( MMFR ) after they had run on a treadmill for eight minutes . There was no significant change in baseline FEV1 or MMFR before each agent was given . Saline , lignocaine , and sodium cromoglycate did not alter the mean baseline FEV1 or MMFR significantly .  Ipratropium  caused bronchodilatation with an increase of 16·3 % in the mean FEV1 ( p<0·001 ) and of 43·4 % in the mean MMFR ( p<0·05 ) . After exercise the maximal percentage falls in FEV1 ( means and SEM ) after saline , lignocaine , sodium cromoglycate , and ipratropium bromide were 38·1 % ( 5·0 ) , 34·5 % ( 6·1 ) , 11·3 % ( 3·7 ) , and 19·3 % ( 7·4 ) respectively . Similarly , the mean maximal falls in MMFR  after saline , lignocaine , sodium cromoglycate , and ipratropium bromide were 54·4 % ( 5·2 ) , 52·9 % ( 7·7 ) , 23·6 % ( 6·6 ) , and 32·1 % ( 10·5 ) respectively . The inhibitory  effects of sodium cromoglycate and ipratropium bromide were significant whereas lignocaine failed to produce an effect . These results suggest that mediator release is an important factor in exercise-induced asthma and that in some patients the effects of the mediators may be on the postsynaptic muscarinic receptors . Local anaesthesia of sensory vagal receptors , on the other h and , does not prevent exercise asthma and these receptors do not appear to have any important role in exercise-induced bronchoconstriction The effects of ipratropium bromide ( 80 and 200 micrograms ) and placebo on the basal bronchial tone and on methacholine-induced bronchoconstriction were investigated in 10 asthmatic patients in a placebo-controlled double-blind manner . Bronchial hyperreactivity to methacholine was confirmed at a pretrial bronchial challenge . The patients were r and omly allocated to two groups in which the drug was inhaled from either metered-dose inhalers ( MDI ) or powder capsules . With the high dosage , the bronchodilation result ing from powder capsules was somewhat more pronounced than that achieved with the MDI . Otherwise the bronchodilator effect of ipratropium bromide and the protection afforded by the drug against methacholine-induced bronchoconstriction were similar in the two groups . In five patients the bronchodilator effect was better and in four patients the tolerance to methacholine was greater after the higher ipratropium dosage than after the lower one . In two patients ipratropium bromide had no bronchodilator effect but gave good protection against methacholine-induced bronchoconstriction . It is concluded that some patients benefit from a dosage of ipratropium bromide higher than that usually recommended and that an anticholinergic effect on the bronchi is possible even in the absence of the bronchodilator effect in the basal state BACKGROUND In acute asthma the optimal duration of treatment with combination β agonist and anticholinergic nebuliser solutions is unknown ; most studies have investigated single doses or treatment for up to 12 hours . To determine whether longer treatment with ipratropium bromide might aid recovery a study was undertaken in 106 patients with acute asthma . METHODS A double blind , r and omised , placebo controlled , three group study was performed with all patients receiving ipratropium for 12 hours and salbutamol for 60 hours after admission ( both nebulised four hourly ) , systemic steroids and , if necessary , theophylline . At 12 hours ipratropium was stopped in group I ( n = 35 ) but was continued in the other two groups , and at 36 hours ipratropium was also stopped in group II ( n = 35 ) while patients in group III ( n = 36 ) continued with ipratropium for 60 hours . Spirometric tests were performed before and after salbutamol , and again 30 and 60 minutes after ipratropium or placebo at 12 , 36 and 60 hours . Peak flow rates ( PEFR ) were measured before and after each nebulisation . RESULTS There were no differences between the groups in PEFR on admission ( group I : 214 l/min , group II : 198 l/min , group III : 221 l/min ) , or mean forced expiratory volume in one second ( FEV1 ) at 12 hours ( group I : 1.8 l , group II : 2.0 l , group III : 2.2 l ) , 36 hours ( group I : 2.1 l , group II : 2.3 l , group III : 2.4 l ) , or at 60 hours ( group I : 2.2 l , group II : 2.3 l , group III 2.5 l ) . Despite this , median time to discharge was significantly higher for patients in group I ( 5.4 days ) than for those in groups II ( 4.1 days ) and III ( 4.0 days ) . CONCLUSIONS Combination nebulised therapy can be continued beyond 12 hours and up to 36 hours after admission with improved recovery time . Lung function testing may not reflect the full benefit of treatment In order to determine the duration of action of the inhaled anticholinergic agent oxitropium bromide , a controlled study of the effect of pre-treatment with oxitropium bromide 200 micrograms against cholinergic challenge was carried out in ten asthmatic subjects ( 6 children , 4 adults ) . After baseline measurements of lung function ( FEV1 and sGaw ) and methacholine PC20 ( the concentration of methacholine to produce a 20 % fall in FEV1 ) oxitropium bromide or placebo were inhaled double-blind on 2 separate days . Lung function and methacholine PC20 were then measured at 1 , 3 and 6 h post dosing . Oxitropium bromide caused significant protection from methacholine challenge for 6 h ( p less than 0.05 ) A multi-center , double-blind , 90-day study compared an ipratropium bromide metered-dose inhaler ( 40 microgram four times a day ) with a metaproterenol metered-dose inhaler ( 1,500 micrograms four times a day ) in 164 patients with asthma ; of the 144 patients who completed the study , 71 received ipratropium and 73 received metaproterenol . Our results suggest that both drugs were equally effective bronchodilators . Although the shape of the pulmonary function response curves suggested that ipratropium has different bronchodilator kinetics than metaproterenol ( in that it has a slower onset of action and a more prolonged duration ) , comparison of the areas under the curves for the two drugs showed that there was no statistical difference between ipratropium or metaproterenol . The only significant side effects noted with ipratropium were cough and exacerbation of symptoms ; no anticholinergic side effects were noted Forty-nine asymptomatic asthmatic children who showed exercise induced bronchospasm ( EIB ) , received in a r and omized double-blind fashion one of the four following drugs administered through nebulizer and facial mask : salbutamol 4 mg ( 13 patients ) , disodium chromoglycate 20 mg ( 12 patients ) , ipratroprium bromide 0.4 mg ( 12 patients ) , placebo ( 12 patients ) . They performed exercise fifteen minutes after receiving the drugs and spirometries were done 0 , 5 , 10 , 15 and 20 minutes after the end of the exercise . Bronchodilation was noticed 15 minutes after the administration of salbutamol and ipratroprium bromide but not after cromoglycate or placebo . No patient receiving either salbutamol or cromoglycate had EIB whereas it occurred in 50 % of those receiving ipratroprium bromide and 91.6 % of those receiving placebo Thirty seven children with acute asthma were given nebulised ipratropium or placebo 30 minutes after their first dose of salbutamol and eight hourly thereafter . There were no significant differences between the two groups in clinical scores , peak expiratory flow rates , length of stay in hospital , or the need for oral steroids Six asthmatic children were studied to determine whether supplemental , parenteral atropine would increase the effects of bronchodilation and protection against exercise-induced bronchoconstriction after maximal effects had been achieved by inhalation . First , we determined the amount of inhaled atropine sulfate that would give maximal bronchodilation for each patient at rest . This quantity of atropine was design ated as " A. " Then all subjects exercised for five sessions with the following pre-exercise treatments in a r and om order : ( a ) inhaled distilled water plus intramuscular ( IM ) saline solution ; ( b ) inhaled A dose of atropine plus IM saline solution ; ( c ) inhaled distilled water plus 0.35 mg IM atropine ; ( d ) inhaled A dose of atropine plus 0.35 mg IM atropine ; and ( e ) inhaled double the A dose plus IM saline solution . The results showed that the combination of inhaled and IM atropine had the greatest bronchodilation effect and the greatest protection against exercise-induced bronchoconstriction .  Atropine inhalation alone ( A dose ) or IM injection ( 0.35 mg ) was not as effective in bronchodilation or in alleviation of exercise-induced bronchoconstriction . Doubling the dose of inhalation ( 2A ) did not increase the effects of the A dose . These results support the hypothesis that inhaled atropine does not reach all the airways where cholinergic receptors are present Until now very few studies have been performed on the prevention of exercise-induced asthma ( EIA ) in children with ipratropium bromide + fenoterol .  This is why we decided to study 30 children aged between 6 and 15 years , whose EIA was confirmed by a test including a 6-min free race on day 1 of the study . The criterion was a decrease of more than 20 % of the basal values of forced expiratory volume in 1 s ( FEV1 ) or FMF .  Children whose FEV1 or FMF baseline values were under 60 % of those expected according to Polgard tables were excluded . Three tests were performed , the first to determine EIA , the second was performed 72 h later after inhalation of placebo . 72 h after day 2 the patients returned in order to repeat the test , but this time , aerosol therapy with the combination ipratropium + fenoterol was applied prior to the race . The dosage of the combination was 1 puff of aerosol per 10 kg body weight , up to a maximum of 4 puffs . Each puff of the combination contains 0.02 mg of ipratropium bromide and 0.05 mg fenoterol . Functional assessment of children was carried out by means of forced spirometry . There were no significant differences between the placebo group and the group which received no medication , but there was a significant difference between the treated group and the other two , not only in the FEV1 and FMF values but also in forced vital capacity TEST . ( ABSTRACT TRUNCATED AT 250 WORDS A number of drugs are known to inhibit exercise-induced asthma ( EIA ) , but the results in some cases have been difficult to interpret due to the techniques employed . A comparative study was carried out in a group of children to investigate the effects of  salbutamol , choline theophyllinate , cromolyn sodium , atropine , and placebo . The exercise test took the form of six minutes of st and ardized treadmill running . All the drugs , but not the placebo , were able to inhibit EIA ti a significant degree , the effect being most marked with salbutamol . Cromolyn sodium caused no bronchodilatation at rest , while all the other drugs were brondhocilators , the effect being most marked with the atropine during exercise . It was impossible to distinguish the type of drug used for inhibition of EIA if it caused bronchodilatation at rest . The manner in which an exercise test can be used to investigate the duration of action or site of action of drugs is noted Glycopyrrolate , a quaternary ammonium anticholinergic compound is a potentially useful bronchodilator . To determine the efficacy , optimal dose , and duration of action of inhaled glycopyrrolate , we gave the drug to 11 asthmatic patients . Each subject received placebo or glycopyrrolate ( 100 , 200 , 600 , or 1,200 micrograms ) by inhalation in a double-blind , r and omized , crossover design . Measurements included FEV1 , FVC , heart rate , and blood pressure before administration of the drug and periodically for 12 hours . For eight hours following all doses of glycopyrrolate , both FEV1 and FVC ( both as percent of predicted ) were significantly greater for drug than for placebo . Glycopyrrolate may be a useful long-acting drug for the treatment of asthma 
    Output:
    