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PubMed2001

Exercise-induced bronchoconstriction among Malay schoolchildren.

OBJECTIVE: Exercise-induced bronchoconstriction (EIB) may be demonstrated in 60-70% of asthmatic children in temperate climates. In areas of high humidity it is postulated to be low. The aim of the study was to determine the prevalence of EIB in a population of schoolchildren with wheezing, living in the humid tropical climate of Kuala Lumpur, Malaysia. METHOD: We performed a cross-sectional study using the International Study of Asthma and Allergies in Childhood questionnaire to identify 7-12-year-old Malay children with asthma symptoms from a primary school in central Kuala Lumpur. Sixty-five of 76 children with 'ever wheeze' performed an exercise challenge test successfully in an uncontrolled environment. A random sample of 80 schoolchildren with no history of wheeze were similarly tested as controls. The relative humidity and temperature were recorded. A fall of > 15% was considered as clinically important. RESULTS: The prevalence of EIB in schoolchildren with 'ever wheeze' was 47.7%. The prevalence of EIB in children with 'current wheeze' was 51.6%. The prevalence of EIB in controls was 7.5%. The relative humidity during the study ranged from 41 to 90%. There was no significant relationship between different humidity levels and EIB (P = 0.58, regression analysis). CONCLUSION: This study demonstrates that EIB is present in asthmatic children despite the highly humid tropical environment.

Asthma, Exercise-Induced↗
PubMed1983

Aerosol treatment of bronchoconstriction in children, with or without a tube spacer.

To assess whether an extension tube between the aerosol source and the patient improves drug-inhalation therapy in children with acute bronchoconstriction, we treated 20 children under double-blind conditions with placebo or terbutaline delivered by a conventional aerosol or an aerosol with a tube spacer. Both terbutaline treatments resulted in a significant increase in forced expiratory volume in one second, as compared with placebo (P less than 0.001), but treatment with the tube-spacer aerosol produced significantly more improvement than did treatment with the conventional aerosol (P less than 0.01). The number of errors in inhalation technique was reduced when the spacer aerosol was used, and this reduction may account for the greater improvement in the children treated with the spacer.

Aerosols↗
PubMed1987

Immediate and delayed bronchoconstriction after exercise in patients with asthma.

Although an immediate asthmatic response after exercise is known to occur in some patients with asthma, the existence of a delayed asthmatic response after exercise is controversial. Accordingly, we studied 53 patients who had an immediate mean (+/- SD) decrease in forced expiratory volume at one second (FEV1) of 36 +/- 13 percent, which was maximal 13 +/- 12 minutes after the completion of treadmill exercise. Eight of these patients also had a delayed asthmatic response (a 32 +/- 5 percent decrease in FEV1 occurring 5.0 +/- 1.8 hours after exercise). During a control day, on which the FEV1 was measured serially but no exercise was performed, the same delayed asthmatic response was observed in all but one patient. This finding suggests that the delayed asthmatic response observed in these patients after exercise was not specifically related to the performance of exercise. We conclude that in patients who have bronchoconstriction immediately after exercise, a second asthmatic response occurring later after the exercise is uncommon.

Adolescent↗
PubMed2002

Effectiveness of screening examinations to detect unrecognized exercise-induced bronchoconstriction.

OBJECTIVE: To determine if a physician-administered physical examination and screening questionnaire accurately detects exercise-induced bronchoconstriction (EIB) in adolescent athletes. STUDY DESIGN: Cross-sectional study of 256 adolescents participating in organized sports from 3 suburban high schools. The number of persons screened positive for EIB by physical examination and questionnaire was compared with the number of persons with EIB diagnosed by a "gold standard" test that consisted of a 7-minute exercise challenge followed by serial spirometry. RESULTS: We diagnosed EIB in 9.4% of adolescent athletes. The screening history identified persons with symptoms or a previous diagnosis suggestive of EIB in 39.5% of the participants, but only 12.9% of these persons actually had EIB. Among adolescents with a negative review of symptoms of asthma or EIB, 7.8% had EIB. Among adolescents with no previous diagnosis of asthma, allergic rhinitis, or EIB, 7.2% had EIB diagnosed by exercise challenge. Persons who screened negative on all questions about symptoms or history of asthma, EIB, and allergic rhinitis accounted for 45.8% of the adolescents with EIB. CONCLUSIONS: EIB occurs frequently in adolescent athletes, and screening by physical examination and medical history does not accurately detect it.

Adolescent↗
PubMed2004

Determinants of the severity of exercise-induced bronchoconstriction in patients with asthma.

AIM: In examining the mechanisms of exercise-induced bronchoconstriction (EIB), it is important to determine which factors most strongly affect the severity of EIB. We determined such factors in patients with asthma by stepwise multiple-regression analysis. METHODS: Twenty-three patients with asthma underwent pulmonary function tests, methacholine provocation test, and sputum induction. Eosinophilic inflammatory indices and airway vascular permeability index (ratio of albumin concentrations in induced sputum and serum) were examined in sputum samples, and then an exercise test was performed by all asthmatics. RESULTS: There was a significant correlation between the severity of EIB and degree of eosinophilic inflammation in induced sputum. Moreover, there was a significant correlation between the severity of EIB and airway vascular permeability index. Although we could not find a significant correlation between the severity of EIB and 1-sec forced expired volume, 20% provocation concentration of (PC20) methacholine tended to be correlated with the severity of EIB. By stepwise multiple-regression analysis, we also found that airway vascular permeability index, eosinophil cationic protein levels in sputum, and PC20 methacholine are independent predictors of the severity of EIB. CONCLUSION: We found that airway vascular hyperpermeability, eosinophilic inflammation, and bronchial hyperreactivity are independent factors predicting the severity of EIB.

Adult↗
PubMed2004

Airway reactivity is a determinant of bronchodilator responsiveness after methacholine-induced bronchoconstriction.

Airway hyperresponsiveness (AHR) is one of the characteristics of asthma and a risk factor for persistent airflow limitation. Poor response to bronchodilator may be a cause of persistent airflow limitation. Multiple factors may determine bronchodilator responsiveness, including airway reactivity to nonspecific bronchoconstrictive agents. If patients with AHR have poor bronchodilator responsiveness, then it could be a potential mechanism for asthma and persistent airflow limitation in these patients. The objective of this study is to assess the relationship between airway reactivity to methacholine and responsiveness to beta-agonist and beta-agonist/anticholinergic combination in a large subject population. A retrospective data analysis was undertaken of 764 consecutive subjects with > or = 20% reduction in forced expiratory volume during the first second of exhalation from total lung capacity (FEV1) after < or = 189 cumulative units of methacholine. The first 382 subjects received 3 inhalations of metaproterenol and the second 382 subjects received 3 inhalations of albuterol and ipratropium combination after > or = 20% reduction in FEV1. Bronchodilator responsiveness was measured as the percent increase in FEV1 after the treatment. Airway reactivity was assessed as the log10 of methacholine dose response slope. In a simple linear regression model, airway reactivity was significantly related to bronchodilator responsiveness. The coefficient of determination (r2) was 0.15 for the whole groups; 0.14 for metaproterenol group and 0.18 for albuterol/ipratropium combination group (all p<0.0001). The regression coefficient (beta) was 14.0 for the whole group; 14.8 and 13.2, respectively, for the two bronchodilator groups. Airway reactivity to methacholine is a determinant of airway responsiveness to both beta-agonist and beta-agonist/anticholinergic combination. Subjects with higher airway reactivity have higher bronchodilator responsiveness.

Administration, Inhalation↗
PubMed2000

Inhaled albuterol, but not intravenous lidocaine, protects against intubation-induced bronchoconstriction in asthma.

BACKGROUND: The ability of intravenous lidocaine to prevent intubation-induced bronchospasm is unclear. The authors performed a prospective, randomized, double-blind, placebo-controlled trial to test the ability of intravenous lidocaine and inhaled albuterol to attenuate airway reactivity after tracheal intubation in asthmatic patients undergoing general anesthesia. METHODS: Sixty patients were randomized to receive either 1.5 mg/kg intravenous lidocaine or saline, 3 min before tracheal intubation. An additional 50 patients were randomized to receive 4 puffs of inhaled albuterol or placebo 15-20 min before tracheal intubation. Anesthesia was induced with propofol. Immediately after intubation and at 5-min intervals, transpulmonary pressure and airflow were recorded, and lower pulmonary resistance (RL) was calculated. Isoflurane was administered after the initial two measurements to assess reversibility of bronchoconstriction. A bronchoconstrictor response to intubation was defined as RL greater than or equal to 5 cm H2O. l-1. s-1 in the first two measurements after intubation and RL subsequently decreasing by 50% or more after isoflurane. RESULTS: The lidocaine and placebo groups were not different in the peak RL before administration of isoflurane (8.2 cm H2O. l-1. s-1 vs. 7.6 cm H2O. l-1. s-1) or frequency of airway response to intubation (lidocaine 6 of 30 vs. placebo 5 of 27). In contrast, the albuterol group had lower peak RL (5.3 cm H2O. l-1. s-1 vs. 8.9 cm H2O. l-1. s-1; P < 0.05) and a lower frequency of airway response (1 of 25 vs. 8 of 23; P < 0.05) than the placebo group. CONCLUSIONS: Inhaled albuterol blunted airway response to tracheal intubation in asthmatic patients, whereas intravenous lidocaine did not.

Administration, Inhalation↗
PubMed1983

Acute bronchoconstriction associated with transtentorial herniation in a patient with elevated intracranial pressure.

A patient with acutely elevated intracranial pressure (ICP) and a severe attack of bronchoconstriction is presented. Further investigation after treating the combined emergency situation revealed uncompensated hydrocephalus. Possible mechanisms which might be responsible for the coexisting emergency states are discussed. The urgent need for immediate simultaneous treatment of both disease entities is emphasized.

Acute Disease↗
PubMed1977

Effects of labetalol and propranolol on histamine-induced bronchoconstriction in normal subjects.

1 The effects of oral propranolol (80 mg), labetalol (400 mg) and placebo on blood pressure, pulse rate and FEV1 at rest and after inhaled histamine, have been compared in six healthy male volunteers. 2 At 90 and 120 min after ingestion propranolol reduced the pulse rate and labetalol reduced the blood pressure, thus confirming absorption of each drug. 3 At 120 min propranolol reduced resting FEV1 and enhanced the fall in FEV1 after histamine, whereas the alterations in FEV1 after labetalol did not differ from placebo. 4 These findings suggest that labetalol is less likely than propranolol to cause bronchoconstriction in asthmatic patients.

Adult↗
PubMed1989

Effect of an inhaled mast cell stabiliser, N-acetyl-aspartyl-glutamate (Zy15109) on allergen-induced immediate bronchoconstriction.

We have studied the effect of a mast cell stabiliser, the magnesium salt of N-acetyl aspartyl glutamic acid (NAAGA) on allergen-induced immediate bronchoconstriction in 12 atopic subjects. Inhaled NAAGA, at a dose of 60 mg thrice daily for 1 week, offered no protective effect on the airways against allergen challenge when compared with a matched placebo. The drug was well tolerated with no adverse effects observed.

Adult↗
PubMed1990

Effects of a PAF-antagonist (BN 52063) on bronchoconstriction and platelet activation during exercise induced asthma.

1. The effects of a specific PAF acether antagonist (BN 52063) on the response to isocapnic hyperventilation with dry cold air (ISH study) and exercise (EIA study) were assessed in a single dose and short term treatment study in 10 patients with exercise induced asthma. 2. ISH challenge was performed twice within 1 h after administration of either placebo, 240 mg BN 52063 p.o. or inhalation of 2.4 mg BN 52063. Hyperventilation increased Raw from 0.30 +/- 0.02 to 0.89 kPa s l-1 (P less than 0.001) after the first challenge and from 0.28 +/- 0.04 to 0.84 +/- 0.06 kPa s l-1 (P less than 0.001) after the second challenge. Oral pretreatment with BN 52063 did not result in a reduction of bronchoconstriction during both challenges. A significant increase of Raw was noted immediately after inhalation of BN 52063. An inhibition of PAF induced platelet aggregation (by a factor of 2) occurred after oral administration of BN 52063 after both ISH challenges (P less than 0.05). No significant inhibition of PAF induced platelet aggregation was seen after inhalation of BN 52063. At concentrations up to 30 microM in vitro, BN 52063 inhibited PAF induced platelet aggregation in a dose dependent manner. The IC50 of BN 52063 against the aggregating effect of 1 microM PAF was 7.0 +/- 2.1 microM. 3. In the EIA study the patients were challenged on the third day of treatment with either placebo or 240 mg BN 52063 p.o. or 5 mg BN 52063 by inhalation. Peak expiratory flow rates (PEFR) fell by 155 +/- 37 1 min-1 after exercise.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗
PubMed1988

Bronchoconstriction due to 8-methoxypsoralen.

A patient with psoriasis developed bronchoconstriction after oral 8-methoxypsoralen given as part of his photochemotherapy with PUVA. It was possible to treat the patient with PUVA whilst he was on prophylactic anti-asthmatic therapy. Twenty one further patients on photochemotherapy were studied in detail and none had evidence of impaired pulmonary function as a result of therapy.

Asthma↗
PubMed1975

Effect of alpha receptor blocking drug, thymoxamine, on allergen induced bronchoconstriction in extrinsic asthma.

In ten patients with extrinsic bronchial asthma, allergen provoked bronchospasm was significantly inhibited by the alpha receptor blocking drug thymoxamine given intravenously. In two of these patients thymoxamine by inhalation also effectively inhibited allergen induced bronchoconstriction. It is suggested that thymoxamine may be acting either by increasing intracellular levels of cyclic AMP and thus inhibiting mediator release following allergen challenge or by modifying the airways response to these mediators by altering the bronchomotor tone. The variable responses recorded after allergen challenge in presence of alpha blockade with thymoxamine suggests that the dominant effect is on the bronchomotor tone rather than the mediator release.

Administration, Intranasal↗
PubMed1979

Acute bronchoconstriction caused by Beclovent and not Vanceril.

A 24-year-old asthmatic patient reported acute wheezing immediately after using an aerosol of beclomethasone dipropionate (Beclovent). She was hospitalised for bronchial challenges. Immediate bronchoconstriction was shown after two puffs of this aerosol and after inhalation of the placebo containing all the products of the aerosol less the beclomethasone. Another brand of beclomethasone aerosol, Vanceril, did not produce any reaction. Since the contents of these two beclomethasone aerosols are similar, the authors suggest that rubber or plastic derivative(s) present in the metering valve might have been responsible for the reaction.

Adult↗
PubMed1979

A controlled study on the preventive effect of ketotifen, an antiallergic agent, on methacholine-induced bronchoconstriction in asthmatics.

We studied the preventive effect of ketotifen, an oral drug with antianaphylactic and antihistaminic properties on methacholine-induced bronchoconstriction in controlled cross-over experiments in twenty-six adult patients with extrinsic asthma. Both a single dose of 1 mg ketotifen and 4 weeks treatment of ketotifen, 1 mg twice daily, failed to reduce the methacholine-induced drop in peak expiratory flow. The spirometric findings remained unchanged during ketotifen treatment. There was no difference between treatments with ketotifen and placebo with regard to the patients assessment of the severity of asthma or airway sensitivity to tobacco smoke, fumes or dusts, or exercise. The results suggest that treatment during 4 weeks with ketotifen does not reduce unspecific broncial hyperreactivity in patients with extrinsic asthma.

Adolescent↗
PubMed1981

The effect of verapamil on histamine and methacholine-induced bronchoconstriction.

Calcium antagonist, verapamil given by inhalation did not alter histamine bronchial hyper-reactivity in ten patients with extrinsic bronchial asthma and similarly did not modify methacholine-induced bronchoconstriction in further five patients. In eight non-asthmatic subjects verapamil reduced histamine sensitivity with increase in PC20H from 8.07(+/- 2.33) to 12.10(+/- 2.71, P less than 0.05) but failed to have an effect on methacholine sensitivity in five controls. The failure of inhaled verapamil to modify histamine and methacholine bronchial hyper-reactivity in asthmatic patients and the beneficial effect of calcium antagonists in exercise asthma suggests that these agents may act predominantly on the mast cell degranulation rather than the bronchial smooth muscle.

Adolescent↗
PubMed1985

Effects of ketotifen on in vitro bronchoconstriction.

We have studied the effects of Ketotifen [Ke] (10(-4)M and 10(-6)M) on two in vitro models of bronchoconstriction: actively sensitized guinea-pig trachea (GPT), and passively sensitized human bronchial muscle (HBM). Experiments were performed on matched pairs of tissues. Cumulative dose response curves [CDRC] for histamine and acetyl choline were constructed, and repeated after pre-incubation with Ke or saline control. The effect of Ke on maximal antigen induced contractions was also studied. Contraction of GPT by histamine and acetyl choline was inhibited by Ke 10(-4)M, though this effect was not apparent at high doses of acetyl choline. Ke 10(-6)M had a weaker inhibitory effect on histamine and acetyl choline induced responses. Contraction of GPT by antigen was unaffected by Ketotifen. In the HBM model, Ke 10(-4)M inhibited acetyl choline and antigen induced responses. Ketotifen, 10(-6)M had an inhibitory effect on acetyl choline induced contractions, though this was small, and not seen at higher agonist doses. Contraction of HBM by antigen was unaffected by Ke 10(-6)M. We were unable to obtain reproducible CD RC's to histamine with HBM. The weaker or absent effects of Ke 10(-6)M, a level close to that obtained in clinical practice, may explain some of the poor results of clinical trials, and suggest that efficacy may be improved by the use of higher doses.

Acetylcholine↗
PubMed1989

The effect of histamine-H1 receptor antagonism with terfenadine on concentration-related AMP-induced bronchoconstriction in asthma.

Selective histamine-H1 receptor antagonists inhibit adenosine 5'-monophosphate (AMP)-induced bronchoconstriction by greater than 80% when expressed as a percentage inhibition of the FEV1 time-response curve following inhalation of the provocation concentration of AMP required to produce a 20% decrease in FEV1 from baseline (PC20). To investigate this further we have determined that, in eight mild atopic asthmatic subjects, terfenadine (180 mg), administered 3 hr pre-challenge, increases the geometric mean PC20 for histamine from 0.4 (range 0.03-3) mg/ml after placebo, to 20.2 (range 0.6-64) mg/ml following active treatment (P less than 0.0001). For AMP, the PC20 increased from 9.3 (range 1.0-113.3) mg/ml after placebo, to 150.2 (range 32.1-1177.7) mg/ml with terfenadine (P less than 0.0001). This 16.2-fold (range, 5.5-47.9) displacement to the right of the AMP concentration-response curve by a selective histamine-H1 receptor antagonist emphasizes the central role of histamine in the airways response to this nucleotide.

Adult↗