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PubMed1989

Selective histamine blockade in childhood asthma; the effect of terfenadine on resting bronchial tone and exercise induced bronchoconstriction.

The orally active histamine H1 blocker terfenadine was investigated for its effect on resting bronchial tone and exercise induced bronchoconstriction in 20 asthmatic children by a double blind placebo controlled study. Terfenadine produced acute broncholidation with an average 32% improvement in FEV1 by 3 h. After exercise challenge terfenadine partially inhibited exercise induced bronchoconstriction. The maximum fall in PEFR after exercise was reduced from 32% after placebo to 21.5% after terfenadine. These results suggest that asthmatic children have background resting 'histamine tone' that is reversible by histamine H1 blockage.

Adolescent↗
PubMed1998

A comparison of the onset of action of salbutamol and formoterol in reversing methacholine-induced bronchoconstriction.

This single-centre, randomized, double-blind, double-dummy four-way cross-over study in 24 moderately severe asthmatic patients compared the speed of onset of recommended doses of salbutamol (200 micrograms) and formoterol (12 micrograms) delivered by metered-dose inhaler in reversing the bronchoconstriction induced by a cumulative dose of methacholine to produce a 20% decrease (PD20) in forced expiratory volume in 1 s (FEV1). Specific airway conductance (SGAW) and airway resistance (RAW) were measured in baseline condition, immediately after challenge and 0.5, 1.5, 3, 5, 10, 15, 30, 60 min and every hour up to 4 h after inhalation of the trial drug. FEV1 was measured in baseline condition, after challenge and 15, 30 and 60 min and then every 30 min up to 4 h after inhalation of the study drug. The primary efficacy parameter was the change in SGAW. Salbutamol produced a two-fold increase in SGAW within 4 min and a maximum increase after 79.3 min. Formoterol produced a two-fold increase in SGAW after 5 min and a maximum increase after 119.6 min. Changes in SGAW were slightly, but consistently, higher during the first 2 h after inhalation of salbutamol, both in absolute values and as a percentage of the maximum response. Differences were significant at 10, 15 and 30 min time points. There was no significant difference between the maximum values of SGAW after the two drugs. Changes in RAW and FEV1 reflected the differences in SGAW. It was concluded that in methacholine-induced bronchoconstriction both formoterol and salbutamol have a very fast onset of action, achieving prechallenge values of SGAW within 3 min, salbutamol being slightly faster than formoterol.

Adolescent↗
PubMed2000

Combining a beta2-agonist with a face mask to prevent exercise-induced bronchoconstriction.

BACKGROUND: In this study, we aimed to test the effect of combining a P2-agonist with a heat- and moisture-exchanging cellulose face mask in patients with bronchoconstriction induced by exercise in cold air. METHODS: Nine allergic, asthmatic patients with a history of adverse reaction to exercise were tested on an ergometric bicycle at a temperature of approximately -10 degrees C. They were in turn given no treatment, given premedication with a beta2-agonist, allowed to breathe through a heat- and moisture-exchanging cellulose face mask, and given both premedication and the face mask. After each treatment regimen, they were subjected to provocation with exercise and cold air. RESULTS: The decrease in FEV, was greatest with no therapy (mean maximal change: 27%), and this diminished when the face mask was used (mean maximal change: 12%,) or premedication with a 32-agonist was given (mean maximal change: 7%); no decrease in FEV1 occurred with the combination of agonist and face mask. CONCLUSIONS: The results suggest that different mechanisms are involved in the pathophysiology of exercise-induced bronchoconstriction (EIB). This finding may be of importance for asthmatic athletes who train and compete in a cold climate and are affected by small changes in their lung function.

Adrenergic beta-2 Receptor Agonists↗
PubMed1985

The effect of verapamil and inspired CO2 on the bronchoconstriction provoked by hyperventilation in normal humans.

Two groups of eight normal subjects were investigated in separate studies to demonstrate the effects of changes in end-tidal PCO2, and of pretreatment with the calcium antagonist drug verapamil, on bronchoconstriction provoked by voluntary hyperventilation. Total respiratory resistance (Ros) was measured by the forced oscillation technique before and after 90 s voluntary hyperventilation. End-tidal PCO2 during hyperventilation was varied by altering inspired CO2 concentration. When end-tidal PCO2 fell during hyperventilation, there was a rise in Ros. This did not occur if end-tidal PCO2 was controlled at a normal resting level during hyperventilation. Specific conductance (sGaw) was measured before and after 90 s voluntary hyperventilation of air. Subjects were treated with oral verapamil or placebo for 2 1/2 days and the effect of hyperventilation on sGaw was reassessed. Verapamil reduced significantly the fall in sGaw caused by hyperventilation. Placebo had no effect. In normal humans, bronchoconstriction provoked by hyperventilating air at ambient temperature and humidity is mediated by the fall in PCO2, and is also reduced by verapamil.

Adult↗
PubMed2000

Salbutamol via Easyhaler is at least as effective as salbutamol via Turbuhaler in the treatment of histamine-induced bronchoconstriction.

The aim of this study was to compare the clinical efficacy and acceptability of salbutamol inhaled via Easyhaler and Turbuhaler multi-dose dry powder inhalers in the treatment of histamine-induced bronchoconstriction. Thirty-two adult patients with asthma and/or bronchial hyper-reactivity were included in the study, which was carried out according to a randomized, double-blind, double-dummy, cross-over design. Histamine challenge test was performed on 2 study days separated by at least 7 days. The challenge test was continued until a > or = 20% fall in forced expiratory volume in 1 sec (FEV1) was achieved. The patients then inhaled a single 100 microg dose of salbutamol from Easyhaler, or from Turbuhaler. FEV1 was assessed by flow-volume spirometry before and after histamine challenge and 1.5, 3, 5, 10, 15, 20, 30 and 60 min after salbutamol inhalation. The primary efficacy variable was the maximum percentage change in FEV1 from the post-challenge value. The secondary efficacy variable was area under the curve (AUC) of FEV1. At the end of the study, acceptability of salbutamol Easyhaler was evaluated using a questionnaire and Easyhaler was also compared with the inhalation device the patient had used earlier. Twenty-six patients completed the study. Both salbutamol Easyhaler and salbutamol Turbuhaler produced a rapid and significant increase in FEV1, with maximum percentage changes being 43.9% (+/-15.3) and 40.5% (+/-21.9) from the post-challenge value, respectively. There were no significant differences between the two inhalation devices in terms of changes in FEV1 or AUC of FEV1. The use of Easyhaler and getting a new dose from Easyhaler was considered to be very easy by 65% and easy by 35% of the patients. None considered it difficult. Of 16 patients who had used Turbuhaler earlier, 19% considered Easyhaler much better, 44% better, and 38% the same as Turbuhaler, and none considered it worse. In conclusion, the results show that salbutamol Easyhaler was at least as effective as salbutamol Turbuhaler in the treatment of histamine-induced bronchoconstriction. In addition, the patients considered Easyhaler very easy or easy to use. The majority of patients who reported Turbuhaler as their own inhaler considered Easyhaler better or much better than Turbuhaler.

Administration, Inhalation↗
PubMed2002

Influence of zafirlukast and loratadine on exercise-induced bronchoconstriction.

BACKGROUND: Airway obstruction induced by physical exercise is a common feature in asthma, and conventional treatments do not offer optimal protection. There is thus a need for additional therapies for optimal control of exercise-induced bronchoconstriction (EIB). OBJECTIVE: The influence of treatment with the antihistamine loratadine and the antileukotriene zafirlukast alone and in combination on EIB was investigated. This combination has previously shown beneficial additive effects in allergen-induced bronchoconstriction. METHODS: In a double-blind cross-over study loratadine (10 mg twice daily) and zafirlukast (80 mg twice daily) were evaluated alone and in combination in 16 nonsmoking patients with mild asthma, previously documented EIB, and airways hyperresponsiveness to histamine. RESULTS: The mean +/- SE maximum decrease in FEV1 after a standardized exercise provocation was 21.6% +/- 3% after placebo, 22.8% +/- 3% after loratadine, 13.9% +/- 2% after zafirlukast (P <.05 vs placebo), and 10.3% +/- 2% after the combination of loratadine and zafirlukast (P <.05 vs placebo). Expressed as the area under the FEV1 percentage change versus time curve, the mean protection produced by zafirlukast and the combination of zafirlukast and loratadine was 57% and 65%, respectively, whereas loratadine alone had no significant protective effect. There was also no significant difference between the effect of zafirlukast alone or in combination with loratadine. CONCLUSION: The study confirmed the beneficial effect of a leukotriene receptor antagonist in EIB but failed to obtain evidence that H1-receptor antagonism alone or together with the cysteinyl-leukotriene 1 receptor antagonist zafirlukast offers a protective effect.

Bronchial Diseases↗
PubMed1985

Specific antagonism of adenosine-induced bronchoconstriction in asthma by oral theophylline.

The airway response to increasing concentrations of inhaled-adenosine and histamine after oral theophylline or matched placebo was studied in nine asthmatic subjects. Changes in airway calibre were followed as sGaw and FEV1 and concentration-response curves constructed. Inhaled adenosine caused concentration-related bronchoconstriction and was four-five times less potent than inhaled histamine. Theophylline, which achieved a mean plasma level of 15.9 and 16.6 micrograms/ml on the histamine and adenosine study days respectively, caused significant increases in FEV1 (17%) and sGaw (41-53%) whereas placebo had no effect. Theophylline also protected the airways against histamine-and adenosine-induced bronchoconstriction. However theophylline had a greater protective effect against adenosine (concentration-ratio 17.4 for FEV1 and 12.8 for sGaw) than against histamine (concentration ratio 5.6 for FEV1 and 5.4 for sGaw (P less than 0.05]. At therapeutic concentrations theophylline is a specific antagonist of the airway effects of adenosine in addition to being a bronchodilator and a functional antagonist.

Adenosine↗
PubMed1985

Inhibition of methoxamine-induced bronchoconstriction by ipratropium bromide and disodium cromoglycate in asthmatic subjects.

We compared the effects of pretreatment with saline, ipratropium bromide, and disodium cromoglycate (DSCG) on bronchoconstriction induced by methoxamine--an alpha-adrenoceptor agonist, in asthmatic subjects. All 12 patients bronchoconstricted in response to methoxamine after saline. The PD20 (the dose of methoxamine causing a 20% fall in forced expiratory volume in 1 s [FEV1]) ranged from 0.3-18 mumol. Ipratropium bromide (200 micrograms administered by aerosol) significantly inhibited (P less than 0.05) the response to methoxamine in all patients without producing significant changes in the mean baseline lung function. The mean PD20 for methoxamine after saline was 6.8 mumol and 95% confidence limits (CL) were 3.6, 12.7 mumol. The mean PD20 for methoxamine after ipratropium bromide was 35.4 (95% CL 28.8, 43.6) mumol. DSCG also produced significant (P less than 0.05) shifts to the right in the methoxamine dose response curves, but did not affect resting airway calibre as measured by the FEV1. The mean PD20 for methoxamine increased from 3.3 mumol (95% CL 1.1, 10.0 mumol) after saline to 25.1 mumol (95% CL 14.1, 44.6) after DSCG pretreatment. These findings suggest that alpha-adrenoceptors in the airways of asthmatic subjects may be located at sites other than smooth muscle--possibly on mast cells but more likely on nerve endings and/or parasympathetic ganglia.

Adult↗
PubMed1988

The contribution of histamine release to bronchoconstriction provoked by inhaled benzalkonium chloride in asthma.

1. To investigate the possibility that benzalkonium chloride-induced bronchoconstriction results from the endogenous release of histamine, we examined the effect of the selective histamine antagonists terfenadine and astemizole, on the airways response to inhaled benzalkonium chloride and histamine in 12 asthmatic subjects. 2. Double-blind concentration- and time-course studies were undertaken, 3 h after treatment with terfenadine or matched placebo. 3. Benzalkonium chloride and histamine caused concentration-related falls in FEV1 in all subjects with benzalkonium chloride being 7.4 times less potent as a bronchoconstrictor agonist than histamine. Terfenadine displaced to the right the benzalkonium chloride and histamine concentration-response curves by 3.7 and 111 fold respectively. Terfenadine attenuated the initial (5 min) bronchoconstrictor response to benzalkonium chloride by 40%. However, over the whole 45 min period, the response was reduced by only 13% compared with 86% inhibition of the response to histamine. 4. In an open study, eight of the 12 subjects undertook a time course study with inhaled benzalkonium chloride after pretreatment with the chemically unrelated histamine antagonist astemizole. Astemizole inhibited benzalkonium chloride-induced bronchoconstriction to an almost identical degree as that achieved with terfenadine. 5. We conclude that the initial bronchoconstrictor effect of benzalkonium chloride is due, in part, to histamine release. However, the majority of the adverse effect relates to other, as yet unrecognised effects of this bacteriocidal substance.

Adult↗
PubMed1988

Effect of a PAF antagonist, BN52063, on PAF-induced bronchoconstriction in normal subjects.

1. The effects of an oral platelet activating factor (PAF) antagonist, BN52063, or matched placebo on inhaled PAF challenge were assessed in a double-blind study in eight normal subjects. 2. PAF (24 micrograms) induced an immediate bronchoconstriction, with a maximum fall in flow at 30% of vital capacity from a partial flow volume manoeuvre (Vp30) of 47.1 +/- 7% (mean +/- s.e. mean) 5 min after inhalation following placebo treatment. Repeated PAF challenges at 15 min intervals resulted in tachyphylaxis of the bronchoconstrictor response. 3. Two hours after the ingestion of BN52063 (120 mg) the maximum bronchoconstriction induced by inhaled PAF was attenuated (35.9 +/- 9% fall at 5 min) with a significant reduction (P less than 0.05) in response after the first and second inhalations. 4. Inhaled PAF induced an immediate neutropenia (73.2 +/- 9% fall 5 min after inhalation) followed by a rebound neutrophilia, which were unaffected by pretreatment with BN52063. 5. Oral ingestion of a dose of BN52063 which is effective in reducing skin responses to PAF gave partial protection against the bronchoconstrictor effect of inhaled PAF in normal subjects.

Adult↗
PubMed1988

Reversal of histamine-induced bronchoconstriction by the H1-receptor antagonist levocabastine: a potential model for efficacy in anaphylaxis.

1. The rate of onset and magnitude of the effect of levocabastine, a potent H1-receptor antagonist, in reversing histamine-induced bronchoconstriction were determined in a double-blind cross-over trial against saline placebo. Histamine was administered by nebuliser so that forced expiratory volume in 1 second (FEV1) was reduced to 80-75% of baseline FEV1 in 10 men with mildly or moderately responsive airways and the effects of intravenous injection of saline or saline + 200 micrograms levocabastine were studied. 2. The maximum rate of recovery of FEV1 was 7[2-10]% min-1 (median [range]) in the first 5 min after levocabastine injection, but only 4[1-7]% min-1 after saline alone (P less than 0.05). 3. The median area under the recovery curve of FEV1 from 0 to 30 min after injection was 405 [228-498]% basal FEV1 X min after levocabastine and 301[98-502]% basal FEV1 X min after saline alone (P less than 0.002). 4. FEV1 returned to 90% of baseline within 30 min in all subjects after levocabastine, but not after saline alone (P less than 0.002). 5. Histamine-induced bronchoconstriction was relieved more quickly by levocabastine than saline alone. This model may have application to the study of drugs used in the treatment of anaphylaxis.

Adult↗
PubMed1979

Preventive effect of ketotifen, a new antiallergic agent, on histamine-induced bronchoconstriction in asthmatics.

The preventive effect of ketotifen, a new drug with anti-histaminic and antiallergic properties, on histamine-induced bronchoconstriction was studied by open assessment in twenty-four adult patients with extrinsic asthma. A single oral dose of 1 mg ketotifen reduced the post-histamine mean drop in peak expiratory flow from 33 to 16% of the basal values (P less than 0.001). After a 4 weeks' regimen of 1 mg ketotifen twice daily the post-drug histamine-induced fall in PEF was further significantly reduced (P less than 0.001). Tests performed after 8 and 12 weeks of treatment showed no additional decrease in bronchial reactivity to histamine. Tests performed 1 week after cessation of treatment showed return of bronchial reactivity to the pretreatment level. The results suggest that a single dose of ketotifen has a marked preventive effect on histamine-induced bronchoconstriction and that this effect is enhanced during continued treatment.

Adolescent↗
PubMed1983

The effect of inhaled verapamil on allergen-induced bronchoconstriction.

In eight patients with extrinsic bronchial asthma the effect of inhaled verapamil (3 and 6 mg) was compared with saline on bronchial challenge with extracts of Dermatophagoides pteronyssinus. There was no significant difference in the baseline FEV1 before and after inhalation of saline or verapamil 2.5 mg/ml. However, verapamil at a higher concentration (5 mg/ml) caused bronchoconstriction in four patients who had to be excluded from the part of the study. Verapamil at both these concentrations failed to have an effect on the allergen-induced bronchoconstriction. These findings suggest that verapamil given by inhalation does not prevent mediator release from the lung mast cells following specific allergen challenge.

Adolescent↗
PubMed2003

Potentiation of allergic bronchoconstriction by repeated exposure to formaldehyde in guinea-pigs in vivo.

BACKGROUND: Indoor formaldehyde (FA) might worsen allergies and be an underlying factor for the increasing incidence and severity of asthma; the exact mechanism, however, remains unclear. OBJECTIVE: The present study examined the effects of repeated exposure to FA on methacholine- and antigen-induced bronchoconstriction in guinea-pigs in vivo. METHODS: First, non-sensitized guinea-pigs were transnasally treated with 0.1 or 1.0% FA or saline three times a week for 6 weeks, and increasing concentrations of methacholine (50, 100, and 200 microg/mL) were inhaled at 5-min intervals. Second, guinea-pigs pre-treated with transnasal administration of FA or saline using the same protocol were passively sensitized with anti-ovalbumin (OA) serum 7 days before antigen challenge. Third, guinea-pigs were actively sensitized with OA and pre-treated with transnasal administration of FA or saline using the same protocol. The lateral pressure of the tracheal tube (Pao) was measured under anesthesia and artificial ventilation. RESULTS: The antigen-induced increase in Pao in actively sensitized guinea-pigs was significantly potentiated by FA exposure in a dose-dependent manner. The dose-response curve of the methacholine-induced increase in Pao in non-sensitized guinea-pigs or of the antigen-induced increase in Pao in passively sensitized guinea-pigs was not altered by FA exposure. Transnasal administration of FA significantly increased the serum anti-OA homocytotropic antibody titre (IgG) as measured by the passive cutaneous anaphylaxis reaction in actively sensitized guinea-pigs. CONCLUSION: The results suggest that repeated exposure to FA worsens allergic bronchoconstriction through enhancing antigen sensitization.

Allergens↗
PubMed1990

Contribution of histamine and prostanoids to bronchoconstriction provoked by inhaled bradykinin in atopic asthma.

Bradykinin, a nonapeptide cleavage product of high molecular weight kininogen, is a potent bronchoconstrictor agonist in asthma; however, its mechanism of action is not known. Since bradykinin has been shown to stimulate mediator release from mast cells and augment the release of prostanoids, we have examined the effect of a selective histamine H1 receptor antagonist, terfenadine and a potent cyclooxygenase inhibitor, flurbiprofen on bronchoconstriction provoked by inhaled bradykinin in asthma. As a bronchial provocation procedure bradykinin challenge was repeatable to within 1 doubling dilution. In nine atopic asthmatic subjects, terfenadine 180 mg, when compared to placebo, increased the geometric mean provocation concentration of inhaled agonist required to reduce FEV1 by 20% of baseline (PC20) from 0.7 to greater than 22.9 mg/ml for histamine (P less than 0.01) and 0.3 to 0.5 mg/ml for bradykinin (P less than 0.01). In a further nine atopic asthmatics, flurbiprofen 150 mg when compared to placebo produced a small but significant protection of the airways against bradykinin, geometric mean PC20 increasing from 0.40 to 0.79 mg/ml (P less than 0.05). We conclude that bradykinin is a potent bronchoconstrictor agonist in asthma, being approximately 9.5 times more potent than histamine in molar terms. Pharmacological intervention with terfenadine and flurbiprofen led to a significant protection of the airways against the constrictor effect of bradykinin but the effect in each case was small. Thus, while histamine and prostanoids may contribute as mediators of bradykinin-induced bronchoconstriction, they are unlikely to account for the majority of the response.

Adult↗
PubMed1989

Synergistic potentiation by captopril and propranolol of bradykinin-induced bronchoconstriction in the guinea-pig.

1. Captopril (30 or 100 micrograms/kg intravenous (i.v.] in anaesthetized artificially ventilated guinea-pigs potentiated bronchoconstrictor responses to bradykinin, but not those to histamine or the thromboxane A2-mimetic U46619. 2. Propranolol (5 mg/kg, i.v.) potentiated bradykinin-induced broncho-constriction. The potentiated responses were further augmented by captopril. 3. The captopril-potentiated responses to bradykinin were inhibited during cyclo-oxygenase inhibition with indomethacin. Bronchoconstrictor responses to bradykinin, but not those to histamine or U46619, were reduced after thromboxane synthase inhibition with dazoxiben. The thromboxane A2 antagonist AH23848 inhibited bronchoconstrictor responses to bradykinin, arachidonic acid or U46619 whereas it did not affect those to histamine. 4. A kininase I inhibitor DL-2-mercaptomethyl-3-guanidinoethyl thiopropanoic acid caused no change in bronchoconstriction caused by bradykinin and did not alter the potentiated responses occurring after captopril. 5. Thus, confirmation has been obtained that bradykinin causes broncho-constriction in the guinea-pig indirectly, by release of eicosanoids. Thromboxane A2 is likely to be the major eicosanoid released, since the bronchoconstrictor effect of bradykinin was blocked by indomethacin, dazoxiben and AH23848. The intensity of the bronchoconstriction appears dependent on sympathetic influences mediated by beta-adrenoceptors. Kininase I, in contrast to kininase II apparently has little role in terminating the effects of bradykinin in the lung.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1970

Role of the vagus nerves in anaphylaxis and histamine-induced bronchoconstrictions in guinea-pigs.

1. The effects of vagotomy on the respiratory responses of guinea-pigs to anaphylactic reactions and to intravenous injections of histamine acid phosphate are described.2. In spontaneously breathing guinea-pigs, vagotomy reduced by 50% or more the decreases in total lung conductance (bronchoconstriction) and the decreases in lung compliance, and almost abolished the rapid shallow breathing due to histamine.3. In paralysed, artificially ventilated guinea-pigs, vagotomy reduced by more than 33% the decreases in total lung conductance, but had little effect on the changes in lung compliance due to histamine.4. In paralysed, artificially ventilated guinea-pigs, vagotomy reduced by 75% the decrease in total lung conductance and halved the decrease in lung compliance due to anaphylaxis.5. We conclude that a vagal reflex is mainly responsible for the rapid shallow breathing due to histamine, and partly responsible for the bronchoconstrictions due to histamine and to anaphylaxis in guinea-pigs. We suggest that "lung irritant receptors" in the bronchial epithelium are the afferent end-organs involved.

Airway Resistance↗