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PubMed1990

Histamine H3 receptors modulate antigen-induced bronchoconstriction in guinea pigs.

The effects of a histamine H3-receptor antagonist on the bronchoconstrictor response to antigen challenge were studied in sensitized guinea pigs. We monitored airway opening pressure as an index of airway caliber, and the provocative dose of intravenous ovalbumin (OA) required to produce 200% increase in airway opening pressure (PD200) was determined. Animals were pretreated with propranolol to inhibit adrenergic bronchodilation. OA (1 to 100 micrograms/kg intravenously) challenge caused significant bronchoconstriction with a PD200 of 28.8 micrograms/kg (geometric mean). The selective H3-antagonist, thioperamide (5 mg/kg intraperitoneally), significantly enhanced the OA-induced bronchoconstriction with the PD200 value decreased to 4.0 micrograms/kg (p less than 0.001). The H2-antagonist, cimetidine (10 mg/kg intraperitoneally), had no significant effect on OA-induced response (PD200, 18.2 micrograms/kg). The H1-antagonist, mepyramine (10 mg/kg intraperitoneally), almost completely blocked the effect of OA, suggesting that OA-induced bronchoconstrictor responses are histamine (H1 receptor) mediated. Thioperamide did not alter the dose-response curve to exogenous histamine (0.3 to 3 micrograms/kg intravenously). We conclude that H3 receptors might play a role in regulation of antigen-induced response in the airways.

Animals↗

PubMed1997

Inhibitory effect of indomethacin on tachyphylaxis in response to acetaldehyde-induced bronchoconstriction in patients with asthma.

BACKGROUND: Acetaldehyde, a main factor in alcohol-induced asthma, causes bronchoconstriction indirectly through histamine release; and tachyphylaxis in response to repeated inhalation of acetaldehyde is observed in patients with asthma. OBJECTIVE: The study was designed to clarify the mechanism of tachyphylaxis in response to acetaldehyde-induced bronchoconstriction. METHODS: We investigated the bronchial response to inhaled acetaldehyde in 10 patients with asthma who were treated with indomethacin in a double-blind, randomized, placebo-controlled, crossover fashion. RESULTS: The mean acetaldehyde concentration causing a 20% fall in FEV1 with placebo increased significantly from 13.0 mg/ml (geometric SEM = 0.115) to 31.1 mg/ml (geometric SEM = 0.069) over a period of 1 hour (p < 0.01), whereas there was a slight but not significant tachyphylaxis during indomethacin treatment. The tachyphylactic effect, expressed as logarithmic value of the second PC20 minus logarithmic value of the first PC20, was significantly (p < 0.05) reduced from 0.380 (0.066) with placebo treatment to 0.148 (0.094) with indomethacin treatment. CONCLUSION: These results suggest an important role of cyclooxygenase pathway products in decreased response to repeated inhalation of acetaldehyde in patients with asthma.

Acetaldehyde↗

PubMed1998

Effect of acyclovir on bronchoconstriction and urinary leukotriene E4 excretion in aspirin-induced asthma.

BACKGROUND: Acyclovir (9-[2-hydroxyethoxymethyl] guanine), an inhibitor of the DNA polymerase of the herpes virus, has been reported to exhibit pharmacologic activity other than antiviral activity, including antiasthmatic effects. OBJECTIVE: This study was designed to investigate the protective effect of acyclovir on airway responsiveness to the sulpyrine provocation test and to investigate whether this protective activity is associated with a reduction in aspirin-induced excretion of urinary leukotriene E4 (u-LTE4 ), a marker of cysteinyl leukotriene (LT) overproduction that participates in the pathogenesis of aspirin-induced asthma. METHODS: We assessed the effects of pretreatment with acyclovir on bronchoconstriction precipitated by inhalation of sulpyrine in 16 adult patients with mild or moderate aspirin-induced asthma; those who were in stable clinical condition and were hyperresponsive to the sulpyrine provocation test were allocated to this study. A double-blind, randomized, cross-over design was used. u-LTE4 was measured by a combined reverse-phase HPLC enzyme immunoassay. RESULTS: Acyclovir protects against aspirin-induced attacks of asthma through mechanisms unrelated to its bronchodilator property but related to the improvement of bronchial hypersensitivity to sulpyrine; protection was nearly complete in all patients (P <.0001). By contrast, after acyclovir, the maximum level of u-LTE4 in patients was significantly lower than that in control subjects (P <. 01). CONCLUSION: Our results suggest that acyclovir is not only an antiviral drug but also an inhibitor of analgesic-induced bronchoconstriction, probably acting by inhibiting the release of cysteinyl LTs.

Acyclovir↗

PubMed1989

Inhaled frusemide is highly effective in preventing ultrasonically nebulised water bronchoconstriction.

A decrease in the osmolarity of the periciliary fluid of central airways is supposed to be the initiating mechanism by which ultrasonically nebulised distilled water (UNH2O) induces bronchoconstriction in asthmatics. It is therefore possible that substances, such as frusemide (F), which, in vitro, interfere with ions and water translocation across the tracheo-bronchial epithelium, can also modify such response. To test this hypothesis, 16 adult asthmatics were challenged with UNH2O after being pretreated with either inhaled F (approximately 28 mg delivered into the mouth) or placebo (the diluent) administered in random order and double-blind by means of a jet nebuliser. F did not modify baseline FEV1 and sRaw but attenuated markedly their changes after UNH2O. Mean max % (95% CI) sRaw increases after placebo and F were 293% (168-419) and 63% (21-104), respectively; mean max % falls in FEV1 were 26% (20-32) and 6% (-1-12). Thus inhaled F is highly effective in preventing UNH2O-induced bronchoconstriction and this unexpected property could have therapeutic implications.

Administration, Inhalation↗

PubMed1998

Measurement of bronchoconstriction using whole-body plethysmograph: comparison of freely moving versus restrained guinea pigs.

We have previously measured pulmonary function in guinea pigs using a double-chambered plethysmograph, however, the question remains regarding the accuracy of the double-chamber to gauge the long-term pulmonary function of late asthmatic response. This may be affected by confounding factors, such as stress on the animal and differences in size of the collar around the neck. Therefore, in this study we compared histamine-induced bronchoconstriction in the same guinea pigs using a single- versus a double-chambered body box. In the double-chambered body box, the specific airway resistance is proportional to time delay between thoracic and nasal flows and measured in cmH2O x s. Whereas, in the single-chambered body box, PenH units (Enhanced Pause) reflect "effort of breathing." This is measured as the pause between inspiration and expiration. Doubling concentrations of histamine (12.5-200 microg/ml dissolved in normal saline) were administered by DeVilbiss nebulizer for 1 min, followed by 1 min suction of residual drug in the chamber, and then the airway resistance was recorded by the computer for the following 3 min. There was a 15-min wash-out period between two doses of histamine. There was no statistically significant difference (p > 0.05) in the PC100 values for histamine between the two methods, however, it was much easier to work with the single-chambered body box in terms of handling the animal and eliminating the possible influence of collar placement on the bronchoconstriction. In conclusion, the data suggests histamine challenges produce equivalent PC100 data in both the double-chambered plethysmograph with sRAW units and single-chambered plethysmograph using the PenH units.

Aerosols↗

PubMed2001

Thin-section CT evidence of bronchial thickening in children with stable asthma: bronchoconstriction or airway remodeling?

RATIONALE AND OBJECTIVES: The authors performed this study to determine if bronchial wall thickening is present in children with moderate to severe asthma during periods free from clinical bronchoconstriction. MATERIALS AND METHODS: The authors obtained low (radiation) dose thin-section computed tomographic (CT) scans in each of 18 control subjects and 21 children with moderately severe but stable asthma. Spirometry was performed on all subjects at the time of CT scanning. Bronchial wall thickness and bronchial wall area were measured, and the percentage wall area (bronchial wall area divided by bronchial cross-sectional area) was calculated. The authors performed best-fit regression analysis of wall thickness and percentage wall area versus bronchial diameter and qualitative analysis of images for bronchial wall thickening. RESULTS: In asthmatic patients, the mean percentage of the predicted forced expiratory volume in 1 second was 0.88 +/- 0.09. The best fit regression line that demonstrated the relationship between wall thickness and bronchial diameter for patients with asthma differed significantly from that for control subjects (P < .005). The regression line that demonstrated the relationship between the percentage wall area and bronchial diameter for patients with asthma differed from that of the control subjects when bronchial wall thickness measurements were used to calculate the percentage wall area (P < .05). Results of qualitative analysis also showed significantly more bronchial wall thickening in asthmatic patients than in control subjects (P < .001). CONCLUSION: Bronchial wall thickening detected at thin-section CT in children with moderately severe asthma cannot be attributed solely to bronchoconstriction and may represent airway inflammation or remodeling.

Adolescent↗

PubMed2006

The role of chemokines in exercise-induced bronchoconstriction in asthma.

BACKGROUND: The pathogenesis of exercise-induced bronchoconstriction in asthma is incompletely understood, and the role of chemokines has not been investigated. OBJECTIVE: To investigate the involvement of the CC chemokines eotaxin, regulated upon activation normal T-cell expressed and secreted (RANTES), thymus and activation-regulated chemokine (TARC), and the CXC chemokine interferon-gamma-inducible protein 10 (IP-10) in exercise-induced bronchoconstriction. METHODS: Four groups were enrolled: asthmatic children with positive (n = 15) and negative (n = 15) responses to exercise, children with cystic fibrosis (n = 14), and healthy children (n = 11). Levels of eotaxin, RANTES, TARC, and IP-10 were determined in plasma before, immediately after, and 6 and 24 hours after exercise challenge using enzyme-linked immunosorbent assay. Transcriptional activity was measured using reverse transcriptase-polymerase chain reaction. RESULTS: Exercise did not induce any significant changes in systemic chemokine levels. A significant difference was observed only in the preexercise IP-10 levels among groups (P = .045). There was a significant difference in peripheral blood eosinophil counts among groups (P = .003). In asthmatic children with a positive response to exercise, there was an inverse correlation between eosinophil counts and eotaxin levels (r = -0.616; P = .01) and between forced expiratory volume in 1 second and TARC levels (r = -0.865; P = .001). Reverse transcriptase-polymerase chain reaction studies did not show any difference in the transcription of the chemokines. CONCLUSIONS: Exercise does not cause any changes in the systemic expression of eosinophilic chemokines. Peripheral blood eosinophils may be a determinant of the exercise response, and eotaxin and TARC may be associated with eosinophil counts and forced expiratory volume in 1 second in children with a bronchoconstrictor response to exercise.

Asthma↗

PubMed1999

Comparison of formoterol, salbutamol and salmeterol in methacholine-induced severe bronchoconstriction.

The onset of the bronchodilating effect of formoterol (12 microg by Turbuhaler) was compared with that of salbutamol (50 microg by Turbuhaler), salmeterol (50 microg by Diskhaler) and placebo in methacholine-induced severe bronchoconstriction. Seventeen subjects with mild-to-moderate asthma completed this randomized, double blind, cross-over, double-dummy study. On four study days, baseline forced expiratory volume in one second (FEV1) was recorded and the subjects were challenged with methacholine until FEV1 fell by at least 30%. Immediately thereafter, the study drugs were inhaled and lung function was assessed for 60 min. The geometric mean time for FEV1 to return to 85% of baseline was 7.2 min with formoterol, 6.5 min with salbutamol, 14.1 min with salmeterol and 34.7 min with placebo (p=0.0001, overall ANOVA). The difference between formoterol and salmeterol was statistically significant (p=0.01); there was no difference between formoterol and salbutamol (p=0.69). In conclusion, formoterol reversed methacholine-induced severe bronchoconstriction as rapidly as salbutamol and more rapidly than salmeterol. Classifying beta2-agonists as "fast"- and "slow"- acting may be supplemental to "short"- and "long"-acting.

Administration, Inhalation↗

PubMed1999

Tolerance to beta-agonists during acute bronchoconstriction.

Previous reports suggest that regular use of beta-agonists does not lead to tolerance to their bronchodilator effects. However, most studies have been conducted in stable asthma. This study investigates whether bronchodilator tolerance can be demonstrated during acute bronchoconstriction. Thirty-four asthmatic subjects were treated with 6 weeks inhaled terbutaline (1 mg q.i.d.), budesonide (400 microg, b.i.d.), both drugs or placebo in a randomized, double-blind, cross-over study. After each treatment methacholine was administered to induce a 20% fall in the forced expiratory volume in one second (FEV1). The response to inhaled salbutamol 100, 100, 200 microg at 5 min intervals) was then measured. Dose-response curves were compared using an analysis of covariance. Pre-methacholine FEV1, the highest pre-methacholine FEV1, the fall in FEV1 induced by methacholine and the logarithm of the provocative dose of methacholine required to induce the 20% fall in FEV1 (PD20) were used as covariates. There was a significantly reduced response to salbutamol after 6 weeks terbutaline treatment: the mean (95% confidence intervals (CI)) area under the dose-response curve was reduced by 36% (24, 47) compared to placebo (p<0.0001). The reduction in bronchodilator response was not affected by concomitant treatment with budesonide. Significant tolerance to the bronchodilator effect of inhaled beta-agonists may be demonstrated when tested during acute bronchoconstriction. Continuous treatment with inhaled beta-agonists may lead to a reduced response to emergency beta-agonist treatment during asthma exacerbations.

Acute Disease↗

PubMed2000

Effects of inhaled steroids on methacholine-induced bronchoconstriction and gas trapping in mild asthma.

According to a recent hypothesis, airway smooth muscle regulates airway calibre mostly at high lung volume, whereas the mucosa and adventitia dimensions dominate at low lung volumes. It was thought that if inhaled steroids decrease the thickness of airway wall in asthma, then forced vital capacity (FVC), which reflects the functional changes at low lung volume, should decrease less during induced bronchoconstriction than flow at high volume. The study was conducted in 31 mild asthmatics under control conditions and during a methacholine challenge before and after 4-weeks treatment with inhaled fluticasone dipropionate (1.5 mg daily, 16 patients) or placebo (15 patients). After fluticasone dipropionate treatment, control forced expiratory volume in one second (FEV1), and maximal flow at 50% of control FVC during forced expiration after a maximal (V'max,50) and a partial inspiration (V'p,50) significantly increased. During methacholine challenge, FVC decreased less than did FEV1 or V'max,50, and so did inspiratory vital capacity compared to V'p,50. Both the provocative dose of methacholine causing a 20% fall in FEV1 and the bronchodilator effect of deep inhalation significantly increased. The latter was assessed by means of the regression coefficient of all V'max,50 plotted against V'p,50. No significant changes in these parameters occurred after placebo. These data show that inhaled steroids remarkably blunt the occurrence of gas trapping during induced bronchoconstriction in mild bronchial asthma, possibly due to their effect on airway wall remodelling.

Administration, Inhalation↗

PubMed2000

Efficacy and duration of action of the antileukotriene zafirlukast on cold air-induced bronchoconstriction.

The objectives of the study were to assess the magnitude of the effect of the leukotriene receptor antagonist, zafirlukast, against cold air-induced bronchoconstriction following the first dose and to assess magnitude and duration after 5 days of dosing. Nineteen patients with asthma were included. In a randomized cross-over design, either zafirlukast 20 mg or 80 mg b.d. or placebo were given over 5 days. Challenges were performed 3 h post first dose and 3, 8, 12 and 24 h post last dose. The authors assessed the provocative ventilation rate necessary to achieve a 10% (PV10) and 20% (PV20) fall in forced expiratory volume in one second. The median PV20 3 h post first dose was 69.1 L x min-1 for zafirlukast 80 mg compared to 40 L x min-1 for placebo (p=0.004). The corresponding median value for zafirlukast 20 mg was 59.9 L x min-1 (p=0.06). At steady state the differences in PV20, between zafirlukast 80 mg and placebo were significant at 8 h and 12 h post last dose. The corresponding difference for zafirlukast 20 mg was statistically significant at 8 h post last dose. The analysis of PV10 yielded compatible results. There was no significant protection 24 h after last dose. This study has demonstrated that zafirlukast offers significant protection against cold air-induced bronchoconstriction in asthma. The degree and duration of protection were dose-dependent. However, there was a large interindividual variability for the protective effect of this leukotriene receptor antagonist.

Administration, Inhalation↗

PubMed2002

A study of the association between exercise-induced wheeze and exercise versus methacholine-induced bronchoconstriction in adolescents.

Among asthmatics, exercise-induced wheeze (EIW) is a frequent symptom, and 40-77% of asthmatics demonstrate exercise-induced bronchoconstriction (EIB). In the North-Trøndelag population-based survey of 8,571 adolescents (YOUNG-HUNT), 26% reported wheeze during the previous 12 months (current wheeze). Of those subjects, 50% reported EIW. The aim of the present study was to investigate the association between EIW and EIB in randomly selected adolescents with EIW as the only or predominant asthma-like symptom, and to relate our findings to results from methacholine bronchoprovocation tests (MT) and measurements of exhaled nitric oxide (ENO). Sixty-three subjects with current wheeze induced by exercise, but not by allergen exposure, were investigated using a treadmill exercise test (ET) and measurements of ENO. Fifty-eight subjects completed a MT on a separate study day. EIB was defined as a fall of >or= 10% in the forced expiratory volume in 1 second (FEV1) after exercise (DeltaFEV1%ex). Twenty-one subjects (33%) had EIB and 33 (57%) had a positive MT. The degree of reported dyspnea during the ET was not correlated to the DeltaFEV1%ex. The correlation between EIB and methacholine-induced bronchoconstriction (MIB) was poor, and the DeltaFEV1%ex was more pronounced in smokers than in non-smokers. Moreover, ENO was not increased in subjects with positive vs. negative ET. Hence, EIW, when reported as the only or predominant asthma-like symptom, was linked to EIB in only one-third of the patients. We conclude that EIW is a poor predictor of EIB in epidemiological studies. The poor correlation between EIB and MIB indicates that these two tests measure different mechanisms of bronchial hyper-responsiveness.

Adolescent↗

PubMed2002

Effects of montelukast on physical performance and exercise economy in adult asthmatics with exercise-induced bronchoconstriction.

Leukotriene antagonists are effective in the treatment of exercise-induced bronchoconstriction. Montelukast is a specific cysteinyl-leukotriene receptor1 antagonist without known effects on the pulmonary vessels, which in theory should be advantageous with respect to gas exchange. In addition to lung function, we investigated the effects of montelukast on parameters of gas exchange and physical performance in 16 asthmatics with exercise-induced bronchoconstriction in a double-blind cross-over placebo-controlled study. Subjects were tested at an ambient temperature of -15 degrees C with a tread mill exercise protocol consisting of consecutive workloads of 80% V'O(2max) (6 min), rest (4 min), 60% V'O(2max) (6 min) and step increments of exercise until exhaustion. Montelukast reduced the maximum post-exercise fall in FEV1 (P < 0.01), improved the running time to exhaustion in 11 of 16 test subjects (one unchanged) (P = 0.03), and reduced the Borg score at exhaustion (P = 0.03) and the breathing frequency after 3 min at 60% V'O(2max) (P = 0.03). V'(O2), V'CO(2), minute ventilation, ventilatory equivalents, respiratory exchange ratio, heart rate and oxygen pulse were not significantly different after montelukast and placebo. We conclude that montelukast has a beneficial effect on physical performance in most adults with exercise-induced asthma without any observed effect on gas-exchange parameters.

Acetates↗

PubMed1999

Nitric oxide limits the eicosanoid-dependent bronchoconstriction and hypotension induced by endothelin-1 in the guinea-pig.

1. This study attempts to investigate if endogenous nitric oxide (NO) can modulate the eicosanoid-releasing properties of intravenously administered endothelin-1 (ET-1) in the pulmonary and circulatory systems in the guinea-pig. 2. The nitric oxide synthase blocker N(omega)-nitro-L-arginine methyl ester (L-NAME; 300 microM; 30 min infusion) potentiated, in an L-arginine sensitive fashion, the release of thromboxane A2 (TxA2) stimulated by ET-1, the selective ET(B) receptor agonist IRL 1620 (Suc-[Glu9,Ala11,15]-ET-1(8-21)) or bradykinin (BK) (5, 50 and 50 nM, respectively, 3 min infusion) in guinea-pig isolated and perfused lungs. 3. In anaesthetized and ventilated guinea-pigs intravenous injection of ET-1 (0.1-1.0 nmol kg(-1)), IRL 1620 (0.2-1.6 nmol kg(-1)), BK (1.0-10.0 nmol kg(-1)) or U 46619 (0.2-5.7 nmol kg(-1)) each induced dose-dependent increases in pulmonary insufflation pressure (PIP). Pretreatment with L-NAME (5 mg kg(-1)) did not change basal PIP, but increased, in L-arginine sensitive manner, the magnitude of the PIP increases (in both amplitude and duration) triggered by each of the peptides (at 0.25, 0.4 and 1.0 nmol kg(-1), respectively), without modifying bronchoconstriction caused by U 46619 (0.57 nmol kg(-1)). 4. The increases in PIP induced by ET-1, IRL 1620 (0.25 and 0.4 nmol kg(-1), respectively) or U 46619 (0.57 nmol kg(-1)) were accompanied by rapid and transient increases of mean arterial blood pressure (MAP). Pretreatment with L-NAME (5 mg kg(-1); i.v. raised basal MAP persistently and, under this condition, subsequent administration of ET-1 or IRL 1620, but not of U-46619, induced hypotensive responses which were prevented by pretreatment with the cyclo-oxygenase inhibitor indomethacin. 5. Thus, endogenous NO appears to modulate ET-1-induced bronchoconstriction and pressor effects in the guinea-pig by limiting the peptide's ability to induce, possibly via ET(B) receptors, the release of TxA2 in the lungs and of vasodilatory prostanoids in the systemic circulation. Furthermore, it would seem that these eicosanoid-dependent actions of ET-1 in the pulmonary system and on systemic arterial resistance in this species are physiologically dissociated.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMed2000

Bronchodilator tolerance and rebound bronchoconstriction during regular inhaled beta-agonist treatment.

There is uncertainty about the development of airway tolerance to beta-agonists and the phenomenon of rebound bronchoconstriction on beta-agonist withdrawal. We have recently completed a study of the regular terbutaline and budesonide treatment in asthma. We report our observations on the effect of starting and stopping terbutaline treatment on morning and evening peak flows. The study was a randomized four-way, double-dummy, cross-over comparison of regular inhaled terbutaline (500-1000 microg four times daily), budesonide, combined treatment and matching placebo. Each treatment was given for 6 weeks following a 4 week single-blind placebo washout. Ipratropium was used for symptom relief. No other asthma medication was permitted during either the treatment or wash-out periods. Evaluable data were obtained from 52 subjects for both placebo and terbutaline treatment. Changes in mean morning and evening peak flows during terbutaline treatment were compared to the baseline peak flows during the last 2 weeks of the preceding washout. The peak flow changes on stopping terbutaline were also analysed. Mean morning peak flow was not significantly different during terbutaline treatment when compared to either baseline or placebo treatment. Evening peak flows were significantly higher during terbutaline treatment [mean increase 23.1 l min(-1) (95% CI = 18.8, 27.4)]. Analysis of the peak flow changes on a day-by-day basis revealed an initial increase in morning peak flows for the first 2 days of treatment of 19.2 and 13.41 min(-1) [increases of 25.0 and 17.31 min(-1) in comparison with the corresponding values during placebo (P<0.01)] followed by a return to baseline. The increase in evening peak flows was also greater for the first 2 days of treatment than for the remainder of the treatment period (P<0.01). On ceasing terbutaline treatment there was a fall in mean morning peak flow below the baseline on the following morning of 21.6 l min(-1) (P<0.05 compared to placebo). The temporary increase in morning peak flows and greater than expected rise in evening peak flows for the first 2 days of treatment suggest the development of tolerance to the bronchodilator effect of terbutaline. Similarly, the fall in morning peak flows on treatment withdrawal suggests rebound bronchoconstriction. These effects are likely to be mediated by downregulation of the beta-receptor during treatment. The clinical significance of these changes is uncertain in view of the stability of overall asthma control during terbutaline treatment, but sudden withdrawal of beta-agonist treatment could conceivably lead to a deterioration in asthma control.

Administration, Inhalation↗

PubMed2001

Effect of a cysteinyl leukotriene antagonist, pranlukast hydrate, on acetaldehyde-induced bronchoconstriction in asthmatic patients.

Acetaldehyde is a main factor of alcohol-induced asthma. We previously reported that the cysteinyl leukotriene (cys-LT) receptor antagonist, pranlukast hydrate, inhibits acetaldehyde-induced airway hyperresponsiveness in guinea pigs. The purpose of this study was to evaluate the involvement of cys-LT on bronchial responsiveness to acetaldehyde in asthmatic patients. We investigated the bronchial response to inhalation of acetaldehyde in 10 asthmatic patients, who were treated with placebo or pranlukast hydrate (225.5 mg), a cys-LT receptor antagonist, twice a day for 1 wk using a double-blind, randomized, placebo-controlled, cross-over design. Although a remarkable improvement of acetaldehyde bronchoconstriction was observed in 3 out of 10 subjects, PC(20)-AcCHO values were identical between placebo [12.0 (GSEM, 1.192) mg/ml] and pranlukast [14.7 (GSEM, 1.245) mg/ml] groups. The changes in bronchial responsiveness to acetaldehyde were similar in the six patients who had never experienced alcohol-induced asthma and the four who had. In conclusion, cys-LTs are not involved in acetaldehyde-induced bronchoconstriction.

Acetaldehyde↗

PubMed2002

Plasma adenosine concentration increases during exercise: a possible contributing factor in exercise-induced bronchoconstriction in asthma.

We investigated whether the level of plasma adenosine (ADO) changed during exercise and whether this could be related to exercise-induced bronchoconstriction. Baseline levels of ADO did not differ, but exercise resulted in higher ADO in patients with asthma than in healthy subjects (86 +/- 35 vs 59 +/- 16 nmol/L; P <.001). In patients with asthma, the increase in ADO was related to decreases in FEV(1) (r (2) = 0.475; P <.05) and SaO(2) (r (2) = 0.693; P <.05). These data suggest that adenosine might be involved in the development of exercise-induced bronchoconstriction.

Adenosine↗

PubMed2003

Exercise-induced bronchoconstriction in children: montelukast attenuates the immediate-phase and late-phase responses.

BACKGROUND: Montelukast, a leukotriene receptor antagonist, attenuates exercise-induced bronchoconstriction. We and others have shown that there is a late-phase response 3 to 8 hours after exercise in a subset of asthmatic patients. OBJECTIVE: We sought to evaluate the protective effect of montelukast on immediate-phase and late-phase responses after exercise challenges. METHODS: Twenty-two atopic asthmatic children aged 7 to 16 years with reproducible exercise-induced bronchoconstriction (minimum of 15% decrease of FEV(1) from baseline) were enrolled in this placebo-controlled crossover study. Exercise challenges were performed while breathing cold dry air, and FEV(1) measurements were taken up to 480 minutes after exercise. Patients underwent exercise challenges on a screening day and 1 week after placebo treatment. Subsequently, after a week with no treatment, pulmonary function was assessed after breathing dry cold air (control day). Finally, an exercise challenge was carried out after a week of treatment with montelukast. RESULTS: Reproducible late-phase reactions occurred in 5 of 22 patients, which correlated with the extent of the immediate response (P <.05). After 1 week of treatment with montelukast, a significant decrease of immediate responses was observed. Montelukast treatment compared with placebo was associated with a lower mean maximum decrease of FEV(1) (mean +/- SEM: 17.3% +/- 2.4% and 35.1% +/- 2.6%, respectively), decrease of the area above the curve (267.8% +/- 42.7%/min and 868.0% +/- 103.8%/min, respectively), and shorter time for recovery (6.9 +/- 1.1 minutes and 30.9 +/- 4.0 minutes, respectively; P <.05). Treatment with montelukast also abolished late-phase responses. CONCLUSION: Once daily treatment with oral montelukast attenuated the immediate-phase response and abolished the late-phase response induced by means of exercise challenge in asthmatic children.

Acetates↗