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At least 487 records · Page 27Linked to original sources

PubMed2000

Effect of inhaled low molecular weight heparin on methacholine-induced bronchoconstriction.

OBJECTIVES: Recent studies have shown that inhaled standard heparin exhibits protection towards various bronchoconstrictor stimuli in asthma including methacholine. Low molecular weight heparins (LMWH) (4000-5000 daltons) have higher bioavailability than standard heparins (12,000-16,000 daltons). It is possible that the anti-asthmatic activity of heparin may be molecular weight-dependent. The purpose of the present investigation was to study the effect of LMWH on methacholine-induced bronchoconstriction and to compare the effect of LMWH with that of standard heparin. SUBJECTS: Fifteen subjects (7 male, 8 female, mean age: 33 +/- 13 years, range: 20-65) with mild asthma were studied. METHOD: Methacholine bronchial provocation tests were performed in a single-blind, crossover, randomized order and repeated 45 minutes after placebo or aerosolized standard heparin (1.000 U/kg) or aerosolized LMWH (Enoksaparin, Clexane, 0.8 mg/kg). RESULTS: There was no significant difference in baseline FEV1 values between study days. The standard heparin and enoksaparin inhibited bronchoconstriction induced by methacholine. The geometric mean log PD20 values after placebo, standard heparin, and enoksaparin were 0.24 +/- 0.57 (1.74) mg/ml, 0.79 +/- 0.59 (6.17 mg/ml), 0.76 +/- 0.57 (5.75 mg/ml), respectively (p < 0.0009). Three subjects in standard heparin group and two subjects in enoksaparin group showed increased hyperreactivity, the others showed decreased bronchial hyperreactivity. The degree of protection offered by standard heparin and enoksaparin did not show any statistical difference. CONCLUSIONS: These data suggest that both inhaled LMWH and inhaled standard heparin play inhibitory roles in methacholine-induced bronchoconstriction.

Administration, Inhalation↗

PubMed2000

[Comparison between repeated antigen and acetylcholine-induced bronchoconstriction in development of airway wall thickness in a chronic guinea pig model of asthma].

Asthma is associated with a chronic remodeling of the airways, but it remains to be elucidated whether repeated bronchoconstriction (BC) influences any structural attributes of the lungs. To investigate the role of repeated BC on the morphology of the airways, we chronically exposed guinea pigs to an aerosol of acetylcholine (ACH) over a period of 6 months. The guinea pigs were challenged with either ACH or saline daily for 10 days and thereafter were challenged once a week. To compare repeated BC with a chronic model of allergic inflammation, an additional group of animals were sensitized to aerosolized ovalbumin (OA) and subsequently exposed with OA. The airway wall area and basement membrane (BM) thickness were measured by standard morphometric techniques. Both airway wall area and BM thickness were significantly increased in OA exposed guinea pigs compared with both saline control and AHC-exposed guinea pigs. Our results suggest that persistent bronchoconstriction and/or allergic airway inflammation in asthmatics may contribute to the thickness of the airway wall observed in this disorder. However, repeated acute bronchoconstriction events may not contribute to the increase in the airway wall or BM thickness.

Acetylcholine↗

PubMed2001

[Effect of ipratropium bromide on histamine-induced bronchoconstriction in subjects with chronic airway obstruction].

Ipratropium bromide (IB), a quaternary derivative of atropine has been extensively recommended as the first bronchodilator to be tried in chronic obstructive pulmonary disease (COPD). Despite the large information concerning IB use, a controversy still persists about the lack of non bronchodilator effects (preventive) of inhaled IB. Therefore, the purpose was: to study the effects of IB (80 micrograms) on histamine-induced bronchoconstriction in moderate airway obstruction due to COPD. From outpatient clinic 9 men aged (mean +/- SEM) 57.9 +/- 2.4 yr with smoking history of 54.6 +/- 5.1 pack-yrs and a mean FEV1 = 1.36 +/- 0.08 liters (47.2 +/- 3.8% predicted) were enrolled to participate in this randomized placebo-controlled double blind cross-over study. Each subject attended on 3 occasions (first visit was control day; logPC20 = -0.54 +/- 0.24 mg/ml; geometric mean [MG] = 0.27 mg/ml) for histamine challenge tests using the tidal breathing method after either 4 puffs of IB or placebo aerosol. IB significantly increased baseline FEV1. A correlation between baseline obstruction (FEV1; FEV1/FVC) and bronchodilation with airway hyperreactivity (logPC20) could not be demonstrated. The major finding was that IB attenuated the histamine-induced bronchoconstriction (logPC20 = -0.15 +/- 0.17 mg/ml; GM = 0.70 mg/ml) in comparison with placebo (logPC20 = -0.76 +/- 0.22 mg/ml; GM = 0.17 mg/ml; p = 0.018; doubling doses: IB = 2.02 +/- 0.68 vs placebo = -0.62 +/- 0.79; p = 0.024). The lack of correlation between bronchodilator response to IB and the shift in logPC20 might indicate an intrinsic protective role of IB against histamine. Both IB and fenoterol completely resolved the final fall in FEV1 after ending the histamine challenge test. In conclusion, IB diminished histamine-induced bronchoconstriction in these subjects with moderate COPD.

Adult↗

PubMed2001

Perception of bronchoconstriction in smokers with airflow limitation.

To our knowledge, no data have been provided as to whether and to what extent dynamic hyperinflation, through its deleterious effect on inspiratory muscle function, affects the perception of dyspnoea during induced bronchoconstriction in patients with chronic airflow obstruction. We hypothesized that dynamic hyperinflation accounts in part for the variability in dyspnoea during acute bronchoconstriction. We therefore studied 39 consecutive clinically stable patients whose pulmonary function data were as follows (% of predicted value): vital capacity (VC), 97.8% (S.D. 16.0%); functional residual capacity, 105.0% (18.8%); actual forced expiratory volume in 1 s (FEV(1))/VC ratio, 56.1% (6.3%). Perception of dyspnoea using the Borg scale was assessed during a methacholine-induced fall in FEV(1). The clinical score and the treatment score, the level of bronchial hyper-responsiveness and the cytological sputum differential count were also assessed. In each patient, the percentage fall in FEV(1) and the concurrent Borg rating were linearly related, with the mean slope (PD slope) being 0.09 (0.06). The percentage fall in FEV(1) accounted for between 41% and 94% of the variation in the Borg score. At a 20% fall in FEV(1), the decrease in inspiratory capacity (Delta IC) was 0.156 (0.050) litres. Patients were divided into three subgroups according to the PD slope (arbitrary units/% fall in FEV(1)): subgroup I [eight hypoperceivers; PD slope 0.026 (0.005)], subgroup II [26 moderate perceivers; 0.090 (0.037)] and subgroup III [five hyperperceivers; 0.200 (0.044)]. By applying stepwise multiple regression analysis with the PD slope as the dependent variable, and other characteristics (demographic, clinical and functional characteristics, smoking history, level of bronchial hyper-responsiveness and sputum cytological profile) as independent variables, Delta IC (r(2)=45%, P<0.00001) and to a lesser extent treatment score (r(2)=17.3%, P<0.0006), and to an even lesser extent age (r(2)=3%, P<0.05), independently predicted a substantial amount (r(2)=65.27%, P<0.00001) of the variability in the Borg slope. Thus acute hyperinflation, and to a lesser extent treatment score and age, account in part for the variability in the perception of dyspnoea after accounting for changes in FEV(1) during bronchoconstriction in patients with chronic airflow obstruction.

Analysis of Variance↗

PubMed1992

[Effect of loratadine--selective antagonist of histamine (H1) receptor--on allergen-induced bronchoconstriction in atopic asthmatics].

The aim of this study was to evaluate the effect of loratadine on allergen-induced bronchoconstriction. The study was performed in 7 asthmatic patients with sensitivity to Dermatophagoides pteronyssinus, 4 women and 3 men. aged from 19 to 37 years. The allergen inhalatory--challenge test was performed according to Chai et al. Early phase of Dermatophagoides pteronyssinus--induced bronchoconstriction appeared in all examined patients, but late phase of bronchial obstruction was observed only in 3 persons. 30 mg orally administered of loratadine have no protect effect on early phase of allergen--induced bronchoconstriction. After loratadine ingestion the late phase of this bronchial obstruction disappeared.

Adult↗

PubMed1992

Attenuation of platelet-activating factor induced bronchoconstriction by nedocromil sodium.

We assessed the effect of nedocromil sodium on bronchoconstriction and airway responsiveness induced by platelet-activating factor (PAF) in eight normal subjects, in a double-blind, placebo-controlled cross-over study. Subjects inhaled PAF by a dosimeter method in 5 doses of 18 micrograms each, separated by an interval of 15 min, (total dose of 90 micrograms). Airway calibre was measured by partial expiratory flow at 30% of vital capacity (Vp30) before and at 1, 3, 5, 10 and 15 min after each dose of PAF. The bronchoconstrictor response was assessed by measuring the area under the curve of the percentage fall in Vp30 over time. There was a significant reduction in PAF-induced bronchoconstriction after nedocromil sodium (1,225 +/- 392 arbitrary units; mean +/- SEM) compared to placebo (2,395 +/- 598; p < 0.01). There was no significant difference in the fall in peripheral neutrophil count measured at 5 min after PAF with nedocromil sodium (48.5 +/- 9.5%) compared to placebo (43.3 +/- 6.8%). In conclusion, nedocromil sodium significantly attenuates PAF-induced bronchoconstriction but not the peripheral neutropenia in normal subjects. Since PAF is not a direct constrictor of human airway smooth muscle, this effect of nedocromil sodium may indicate inhibition of release of bronchoconstrictor mediators.

Administration, Inhalation↗

PubMedDate not supplied

Protection against histamine-induced bronchoconstriction by loratadine.

In a simple blind pilot study we have examined the protective effect of loratadine, a new H1 histamine receptor antagonist, against bronchoconstriction induced by histamine inhalation. Six patients with an episodic or continuing obstructive bronchial disease and proven bronchial hyperreactivity were submitted to two identical histamine challenges, first without premedication and then after three days' treatment with 10 mg loratadine daily. The mean FEV1 fall in the first test after histamine inhalation was 33% and in the second test after pretreatment with loratadine only 3.3% (p less than 0.01). Five out of six patients have shown complete protection against histamine-induced bronchoconstriction, in one patient the protection was partial. We conclude that loratadine effectively inhibits histamine-induced bronchoconstriction and could be useful in the prophylactic treatment of asthma and obstructive bronchitis.

Adult↗

PubMed1992

[Effect of atropine and pirenzepine on bronchoconstriction during vagus nerve stimulation in dogs].

The effects of atropine or pirenzepine on bronchoconstriction and reduction in heart rate during vagus nerve stimulation were studied in 10 anesthetized dogs. The bronchoconstriction produced by electrical stimulation of the vagus nerves, 5 min after intravenous injection of atropine or pirenzepine, was recorded as an increase in pulmonary inflation pressure. Atropine and pirenzepine at the doses of 0.01 mg.kg-1 and 0.2 mg.kg-1 respectively were administered and supplemented twice at 30 min intervals. Atropine inhibited the reduction in heart rate more than pirenzepine at all doses. Pirenzepine inhibited the increase in pulmonary inflation pressure more than atropine. Our results suggest that pirenzepine which inhibits bronchoconstriction is useful in patients with bronchial asthma and/or COPD as an anticholinergic agent.

Animals↗

PubMed1992

Protective effect of loop diuretics, piretanide and frusemide, against sodium metabisulphite-induced bronchoconstriction in asthma.

We determined whether the loop diuretic, piretanide, had a similar inhibitory action against sodium metabisulphite (MBS)-induced bronchoconstriction in asthmatic subjects as frusemide and, if so, its duration of action. In the first study, we compared the effect of inhaled placebo, piretanide (24 mg), or frusemide (40 mg), on the provocative concentration of MBS needed to cause a 20% fall in baseline forced expiratory volume in one second (FEV1) (PC20MBS) in 12 mild asthmatic subjects before, immediately after, and at 1.5, 3, 6, and 24 h, after inhalation. Both piretanide and frusemide induced a significant diuresis lasting at least 24 h. Frusemide caused a mean 3.8 fold (95% confidence interval: 2.3-6.3 fold), piretanide a 2.5 fold (1.8-3.4 fold) and placebo a 1.7 fold (1.5-1.9 fold) increase in PC20MBS. The effects of frusemide and piretanide were significantly greater than that of placebo. At later time points, tachyphylaxis to the bronchoconstrictor effects of MBS was observed during the placebo limb. In the second study, we measured PC20MBS at 90 min after inhalation of either placebo, piretanide (24 mg), or frusemide (40 mg). No significant difference in PC20MBS was observed. We conclude that piretanide in addition to frusemide significantly inhibits MBS-induced bronchoconstriction and that this action is short-lived over less than 90 min. Frusemide was more potent in inhibiting MBS-induced bronchoconstriction despite causing a smaller diuretic effect than piretanide. The basic mechanism of action of the loop diuretics in the airways remains unclear.

Administration, Inhalation↗

PubMed1992

The relative contributions of histamine and prostanoids to bronchoconstriction provoked by isocapnic hyperventilation in asthma.

It has been proposed that exercise provokes bronchoconstriction in asthma by inducing mast cell degranulation, and that this occurs secondary to the hyperpnoea of exercise causing hypertonicity of the airway lining fluid. We investigated the contribution of the mast cell products, histamine and prostaglandins, to the bronchoconstriction induced by isocapnic hyperventilation (ISH) using single doses of terfenadine, a specific histamine H1-receptor antagonist, and flurbiprofen, a potent cyclooxygenase inhibitor. We also investigated the effect of flurbioprofen in single dose on bronchial histamine reactivity. Eleven asthmatics took part in a two phase, double-blind, randomized study. In phase 1, subjects attended on three occasions and received either terfenadine 180 mg, flurbiprofen 150 mg, or placebo, prior to 6 min of ISH. The mean maximum percentage fall in forced expiratory volume in one second (FEV1) induced by ISH was 31.5(+/- 3.2)% following placebo, 29.7(+/- 4.4)% following flurbiprofen (NS), and reduced to 16.6(+/- 3.7)% following terfenadine (p less than 0.01). In phase 2, subjects received bronchial challenge with histamine following either flurbiprofen 150 mg or placebo. No significant change in bronchial reactivity following flurbiprofen was seen. We conclude that as administered in this study, flurbiprofen has no effect on baseline bronchial reactivity to histamine. The inhibitory effect of terfenadine indicates that histamine, probably from airway mast cells, makes an important contribution to bronchoconstriction induced by isocapnic hyperventilation, whereas prostaglandin release has no significant role.

Adolescent↗

PubMed2005

Met-enkephalin effects on histamine-induced bronchoconstriction in guinea pigs.

We investigated the effects of the neuropeptide met-enkephalin on histamine-induced bronhoconstriction in an experimental model of asthma. Classic Konzett and Rössler's method of whole body plethysmography modified by Gjuris, was applied in the study. This method represents a standard experimental model of bronchoconstriction, suitable for the evaluation of peptide effects on the histamine-induced bronchoconstriction. The results of the measurements implicate a dose-related modulatory effect of met-enkephalin on the bronchoconstrictor action of histamine. Met-enkephalin doses of 1 mg/kg and 10 mg/kg, respectively, caused statistically significant reduction of the histamine-induced bronchoconstriction. Estimated ED50 dose was 0.235 mg/kg. Further studies are needed to define practical and therapeutical use of the presented observations in respiratory pharmacology.

Animals↗

PubMed1991

[Mechanism of ethanol-induced bronchoconstriction in Japanese asthmatic patients].

Acute ingestion of alcoholic beverages causes no changes in the expiratory airflow rates of most Occidental asthmatic patients. However, asthmatic symptoms are worsened after drinking small amounts of alcohol in Japanese asthmatic patients. Our laboratory results showed that the ingestion of pure ethanol caused a fall in FEV1.0 in about half of the Japanese asthmatic patients tested. The mechanism of ethanol-induced bronchoconstriction remains unclear. In order to investigate this mechanism, we performed oral-provocation tests with 10% ethanol in vivo, and leukocyte histamine release assay induced by ethanol and acetaldehyde in vitro. 55% of asthmatics showed a significant fall in FEV1.0 after ingestion of 10% ethanol (responder). There was no difference in the rise of blood ethanol concentration between the responder group and non-responder group. Acetaldehyde and histamine concentration in the responder group were significantly higher than in the non-responder group. Leukocyte histamine release assay showed that acetaldehyde (2 microM-100 microM) caused dose-dependent histamine release, whereas, ethanol (2 mM-100 mM) had no effect on histamine release. Our data indicate that histamine release from mast cells (or basophils) caused by acetaldehyde may play an important role in ethanol-induced bronchoconstriction. This is the first report on the mechanism of ethanol-induced bronchoconstriction in Japanese asthmatic patients.

Alcoholic Beverages↗

PubMed1990

[Bronchoconstriction in isocapnic hyperventilation-induced asthma].

It is well known that some asthmatic patients develop bronchoconstriction after exercise challenge (exercise-induced asthma, EIA). Recently, it has been pointed out that isocapnic hyperventilation also induces similar bronchoconstriction (hyperventilation-induced asthma, HIA) in the same asthmatic subjects. However, the mechanism of HIA has not yet been determined. In the present study, we performed exercise and hyperventilation challenge in the same patients and pulmonary function data and neutrophil chemotactic factor (NCF) in peripheral blood were examined before and after both challenges. Twelve asthmatic patients with normal pulmonary function data on testing days were subjected to exercise test on a bicycle ergometer and then isocapnic hyperventilation tests in subsequent days. Subjects breathed dry air from the cylinder. Isocapnic hyperventilation was performed by monitoring minute ventilation and each patient followed the same minute ventilation exercise. The reduction of FEV1.0 and time course of airway obstruction were almost the same after exercise and hyperventilation testing. All patients who developed EIA also developed HIA and other patients did not develop both EIA and HIA. Changes of Rrs, V50 and V25 and their time course after each test were also similar in EIA(+) and HIA(+), and in EIA(-) and HIA(-). NCF increased significantly after both challenges in EIA(+) and HIA(+) patient, although increment of NCF was much less these the increases of HIA(+). These data may suggest that the development of bronchoconstriction was compatible after exercise and hyperventilation in each asthmatic patient, however, the mechanism of HIA may differ from EIA, although NCF slightly but significantly increased in HIA, suggesting the possible role of a chemical mediator.

Adolescent↗

PubMed1994

Inhibitory effect of epinastine on bronchoconstriction induced by histamine, platelet activating factor and serotonin in guinea pigs and rats.

Effects of epinastine ((+/-)-3-amino-9,13b-dihydro-1H-dibenz[c,f]imidazo[1,5-a]azepine hydrochloride, WAL 801 CL, CAS 80012-43-7) and reference drugs on bronchoconstriction induced by histamine, platelet activating factor (PAF) and serotonin were studied in guinea pigs and rats. Oral administration of epinastine resulted in a potent inhibition on bronchoconstriction induced by all three bronchoconstrictor agents, and especially, an inhibitory effect on histamine-induced response was remarkable. The effect of epinastine was stronger than that of ketotifen in inhibiting the responses induced by both PAF and serotonin. However, the extent of inhibition in the latter was less remarkable than that seen after histamine. Azelastine was 1.36-4.57 times less potent than epinastine in inhibiting the bronchoconstriction induced by either bronchospasmogen. Although promethazine displayed inhibitory effects on the responses induced by histamine, PAF and serotonin, the inhibiting potency was distinctly inferior to that of epinastine.

Airway Resistance↗

PubMed1993

Effects of bronchoconstriction on the cough reflex in the cat.

The present study was aimed to analyse the influence of bronchoconstriction (Carbachol, 10 micrograms/kg, i.v.) on the cough response to mechanical stimulation of the tracheal mucosa. Experiments were performed in anaesthetised and spontaneously breathing cats, using the isolated glottis technique. Airflow, pleural pressure, subglottic pressure, blood pressure and total lung resistance were recorded. During bronchoconstriction, the cough response was inhibited significantly as shown by the decrease in the number of cough efforts (p < 0.001), in maximum flow during inspiratory (p < 0.001) and expiratory (p < 0.001) movements and in the change of the expiratory (p < 0.01) and inspiratory (p < 0.01) pleural pressures. The mechanical stimulation of the tracheal mucosa evoked always a prolonged decrease of the larynx resistance, including those cases with inhibition of the cough. This study shows that the activation of some type of receptors during bronchoconstriction can modify the cough response to mechanical stimulation of the tracheal mucosa. On the other hand, the widening of the glottis, an associated component of the cough response, can be obtained separately, suggesting that the laryngeal response is centrally integrated via different mechanisms.

Airway Resistance↗

PubMed1993

Differential blockade by tachykinin NK1 and NK2 receptor antagonists of bronchoconstriction induced by direct-acting agonists and the indirect-acting mimetics capsaicin, serotonin and 2-methyl-serotonin in the anesthetized guinea pig.

This study has examined the abilities of (+/-)-CP96345 and (+/-)-SR48968, nonpeptide antagonists selective for the tachykinin NK1 and NK2 receptors, respectively, to block bronchoconstriction caused by intravenous administration of direct-acting receptor agonists and the indirect-acting mimetics capsaicin, serotonin and 2-methyl-serotonin in the anesthetized guinea pig. The NK1 antagonist (+/-)-CP96345 was found to cause, at a maximally tolerated dose of 9 mumol/kg, an approximate 10-fold rightward shift of the dose-response curves for selective NK1 agonists substance P (SP), [Sar9,Met(O2)11]SP and Ac-[Arg6,Sar9,Met(O2)11]SP6-11 without altering responses to selective NK2 agonists neurokinin A (NKA), [Nle10]NKA4-10 or [beta-Ala8]NKA4-10. The NK2 antagonist (+/-)-SR48968 caused dose-dependent rightward shifts of the dose-response curves for the NK2 but not the NK1 agonists. Results using combinations of the receptor antagonists indicate that the NK2 agonists could cause bronchoconstriction by acting on the NK1 receptors at large doses relative to those used without antagonists. Of the agonists used here, [beta-Ala8]NKA4-10 appeared to be the most selective for the NK2 receptors. When used alone, only (+/-)-SR48968 was found to block bronchoconstriction caused by capsaicin, serotonin (after blockade of 5-HT2 receptors by LY53857) and 2-methyl-serotonin. When (+/-)-CP96345 was also given, larger additional blockade was seen with capsaicin than with serotonin or 2-methyl-serotonin as mimetic substance. Atropine caused small and variable degrees of blockade of serotonin and 2-methyl-serotonin but not of capsaicin after combinations of the two antagonists.(ABSTRACT TRUNCATED AT 250 WORDS)

Amino Acid Sequence↗

PubMed1993

Inhibition of antigen-induced bronchoconstriction and eosinophil infiltration in the guinea pig by the cyclic AMP-specific phosphodiesterase inhibitor, rolipram.

Selective inhibition of the low Km cyclic AMP-specific phosphodiesterase has been shown to inhibit inflammatory cell function and relax airway smooth muscle. These studies were conducted to characterize the bronchodilator and anti-inflammatory activity of rolipram, an archetypical cyclic AMP-specific phosphodiesterase inhibitor, in in vitro and in vivo guinea pig airway models. In isolated tracheal rings from ovalbumin (OA)-sensitive guinea pigs, both R- and S-enantiomers of rolipram (1 microM) significantly antagonized OA-induced contractions. In contrast, neither enantiomer at concentrations up to 1 microM significantly inhibited histamine- or LTD4-induced contractions. In superfusion and mediator release experiments, both enantiomers of rolipram significantly reduced antigen-induced prostaglandin D2 release, but had minimal effect on histamine release. In anesthetized, ventilated OA-sensitive guinea pigs, racemic rolipram or enantiomers reduced OA-induced bronchoconstriction with ID50 values of approximately 0.25 mg/kg i.v. Histamine- and leukotriene D4-induced bronchoconstriction were not affected by doses of rolipram which abolished the response to OA. Higher doses (3-10 mg/kg) reduced histamine-, but not the leukotriene D4-induced bronchoconstriction. In conscious OA-sensitive guinea pigs, intragastric pretreatment with rolipram dose-dependently reduced both the OA-induced decreases in specific conductance as well as the corresponding pulmonary eosinophil influx as assessed by both bronchoalveolar lavage and histological evaluation. Therefore, rolipram produces significant inhibition of antigen-induced bronchoconstrictor and inflammatory responses, thus providing strong evidence that this pharmacological approach may be of significant therapeutic value in allergic asthma.(ABSTRACT TRUNCATED AT 250 WORDS)

Anesthesia↗

PubMed1995

Endothelin-induced bronchoconstriction in perfused rat lungs is partly mediated by thromboxane.

In isolated rat lungs, perfusion with either endothelin-1 (ET-1) or the ETB receptor agonist IRL 1620 caused a slowly developing and long-lasting bronchoconstriction. This bronchoconstriction was partly attenuated by the thromboxane receptor antagonist BM 13177. Our data suggest that thromboxane partly mediates this process, together with further unknown mechanisms responsible for ET-induced bronchoconstriction.

Animals↗