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At least 163 records · Page 9Linked to original sources

PubMed1998

Evidence for mast cell activation during exercise-induced bronchoconstriction.

Controversy remains about the causative mediators in the bronchoconstrictive response to exercise in asthma. This study examined whether mast cell activation is a feature of exercise-induced bronchoconstriction by measuring urinary metabolites of mast cell mediators. Twelve nonsmoking subjects with mild asthma and a history of exercise-induced bronchoconstriction exercised on a stationary bicycle ergometer for 5 min at 80% maximum work load. Pulmonary function was monitored and urine was collected before and 30 and 90 min after the provocation. The urinary concentrations of the mast cell markers 9alpha,11beta-prostaglandin (PG)F2 and Ntau-methylhistamine, as well as leukotriene E4 (LTE4) were determined by immunoassay. Seven of the 12 subjects (responders) experienced bronchoconstriction (>15% fall in the forced expiratory volume in one second) following exercise, whereas the pulmonary function of the remaining five subjects (nonresponders) remained stable. The urinary excretion (mean+/-SE) of 9alpha,11beta-PGF2 in the responders increased significantly compared with the nonresponders at 30 (77.1+/-14.4 versus 37.2+/-5.6; p<0.05) and 90 min (79.3+/-8.6 versus 40.4+/-8.5, p<0.05) after exercise challenge. The urinary excretion of Ntau-methylhistamine and LTE4 was not significantly different between the two groups at 30 or 90 min after exercise. The findings represent the first documentation of increased urinary levels of 9alpha,11beta-prostaglandin F2 in adults following exercise challenge and provides clear evidence for mast cell activation during exercise-induced bronchoconstriction in asthmatics.

Adult↗

PubMed1998

Subthreshold concentration of endothelin-1-enhanced, capsaicin-induced bronchoconstriction in anaesthetized guinea-pigs.

An increasing number of studies have been performed to address a possible role for endothelin-1 (ET-1) as a significant mediator in asthma. However, the effects of subthreshold concentrations of ET-1, which cannot elicit bronchial smooth muscle contraction itself, in asthma has yet to be determined. This study determined these effects of ET-1 on capsaicin-induced bronchoconstriction in anaesthetized guinea-pigs. Aerosolized ET-1 administered at doses of 10(-9) M and higher induced a dose-dependent increase in pulmonary resistance, but ET-1 at 10(-10) M did not have any bronchoconstrictive effect. However, this subthreshold concentration of ET-1 potentiated capsaicin-induced bronchoconstriction. In addition, the potentiation of capsaicin-induced bronchoconstriction by this subthreshold concentration of ET-1 was completely abolished by BQ788 (ET(B) receptor antagonist), but not BQ123 (ET(A) receptor antagonists). Immunoreactive substance P (SP) levels in bronchoalveolar lavage fluid after capsaicin administration were significantly higher than those after solvent administration. However, ET-1 alone did not significantly stimulate immunoreactive SP release and ET-1 (10(-10) M) did not potentiate capsaicin-induced immunoreactive SP release. In contrast, ET-1 (10(-10) M) potentiated exogenous neurokinin A- and SP-induced bronchoconstriction. These findings suggest that a subthreshold concentration of endothelin-1 does not potentiate the tachykinin release induced by capsaicin but the airway smooth muscle contraction through endothelin-B receptors.

Aerosols↗

PubMed1997

[Effect of a novel tachykinin NK-2-receptor antagonist, TAC-363, on bronchoconstriction and airway hyperresponsiveness in guinea pigs].

We examined the effect of a novel tachykinin NK-2-receptor antagonist, N alpha-(tert-Butylcarbamoyl)-L-glutaminyl-L-tryptophyl-alpha-aza- phenylalanine 2-benzyloxyethylamide (TAC-363), on hyperventilation- and citric acid-induced bronchoconstriction and neurokinin A (NKA)-, capsaicin- and antigen-induced airway hyperresponsiveness in guinea pigs. The i.v. administration of TAC-363 at doses of 0.01-1 mg/kg inhibited hyperventilation- and citric acid-induced bronchoconstriction in a dose-dependent manner, while FK-888, a tachykinin NK-1-receptor antagonist, did not inhibit hyperventilation-induced bronchoconstriction. NKA-induced airway hyperresponsiveness to acetylcholine was attenuated by i.v. injection of TAC-363, but not by the thromboxane A2 synthetase inhibitor ozagrel and the mast cell stabilizer DSCG. Furthermore, TAC-363 prevented the occurrence of capsaicin- and antigen-induced airway hyperresponsiveness to acetylcholine, while FK-888 did not prevent occurrence of capsaicin-induced airway hyperresponsiveness. In summary, TAC-363 inhibits bronchoconstriction and airway hyperresponsiveness induced by various stimuli. These results suggest that NKA mediates bronchoconstriction and airway hyperresponsiveness. Thus, TAC-363 is expected to be useful in the treatment of airway diseases such as asthma.

Animals↗

PubMed1996

Bronchoconstriction due to cold weather in COPD. The roles of direct airway effects and cutaneous reflex mechanisms.

To clarify how cold weather may induce bronchoconstriction in patients with COPD, a series of challenges were performed in 20 patients with COPD in stable condition as well as in 13 healthy subjects. A whole-body exposure to -17 degrees C during resting nasal breathing was performed to study the reflex effects of facial cooling on lung function. In addition, a near-maximal hyperventilation of cold air was performed in a warm room to study the direct airway effects of cold air. The whole-body exposure to cold air induced statistically significant bronchoconstriction in both groups, the maximal decrements in FEV1 being 9.4 +/- 1.4% in the patients with COPD and 10.3 +/- 0.8% in the healthy subjects (p = NS). The whole-body exposure to cold air also increased the resting ventilation. The hyperventilation challenge induced bronchoconstriction only in the patients with COPD, the maximal decrements in FEV1 being 8.0 +/- 1.3% and 1.5 +/- 1.0%, respectively (p < 0.01). These results suggest that cooling of the facial skin is predominantly responsible for the bronchoconstriction due to cold weather both in patients with COPD and in healthy subjects. At high ventilation level, as during heavy exercise, the direct airway effects of cold air may also contribute to the bronchoconstriction in patients with COPD. Some patients with severe COPD might benefit from wearing protective clothing over their face in cold weather.

Adult↗

PubMed1999

Exercise-induced bronchoconstriction in adults with asthma--comparison between running and cycling and between cycling at different air conditions.

The bronchial response to cycling and running was compared in six adult asthmatic persons. The effects of different air conditions during cycling regarding the induction of bronchoconstriction was studied. The exercise consisted of 6 minutes' work at an intensity of 80-85% of maximal heart rate. Heart rate, oxygen consumption and ventilation were measured to check that the exercise level was the same in all tests. Peak expiratory flow (PEF) was used to test for bronchoconstriction. Bicycling and treadmill running were performed under indoor conditions and bicycling while breathing cold, dry air (-18 degrees C) and room-tempered humid air (60% RH), respectively. No difference in bronchoconstriction was found between cycling and running under indoor conditions. However, bicycling exercise with inhalation of cold dry air provoked more bronchoconstriction than when inhalating humid air (PEF reductions of 19.4+/-6% and 6.1+/-2%, respectively). No differences were found between the exercise modes in heart rate, oxygen consumption, ventilation per minute, respiratory rate, carbon dioxide elimination or subjective ratings of perceived exertion and breathlessness. It is concluded that it is not the type of exercise, but the ventilation demand and humidity of the inspired air that are the main determinants of the occurrence and degree of bronchoconstriction.

Adult↗

PubMed1990

Bronchoconstriction induced by spirometric maneuvers in patients with bronchial asthma.

We analyzed forced expiration maneuver-induced bronchoconstriction in 14 asthmatic patients and in seven normal subjects by breaking down the forced expiration maneuver of spirometry (the FVC maneuver) into two phases: a slow, deep inspiration to the total lung capacity (TLC) (the DI maneuver) and a forced expiration to the residual volume (RV) (the PFV maneuver). Specific airway conductance (sGaw) was measured at functional residual capacity (FRC) after each of the three maneuvers. All of the maneuvers caused the greatest bronchoconstriction immediately after completion of the maneuver. The mean decreases in the sGaw immediately after the FVC, DI, and PFV maneuvers were 45.0 +/- 6.6 (SD)% (P less than .001), 29.6 +/- 5.3% (P less than .001), and 16.7 +/- 5.3% (P less than .03), respectively. The decrease in sGaw by the FVC maneuver was very close to the combined algebraic sum of the DI maneuver and the PFV maneuver. The normal subjects did not show any changes in the sGaw by any of the maneuvers. The inhalation of albuterol almost abolished the response of bronchoconstriction to any of the three maneuvers, but inhalation of an anticholinergic agent, ipratropium bromide, did blunt the response. This study suggests that forced expiration maneuver-induced bronchoconstriction in asthmatics can be caused not only by deep inspiration to the TLC but also by forced expiration to the RV, and that the bronchoconstriction may be brought about mainly by an increase in parasympathetic activity.

Adult↗

PubMed1995

Inhibitory effect of terfenadine, a selective H1 histamine antagonist, on alcoholic beverage-induced bronchoconstriction in asthmatic patients.

We wanted to evaluate the effect of terfenadine, a selective H1-receptor antagonist, on alcoholic beverage-induced bronchoconstriction. Eight patients with alcohol-induced asthma received terfenadine (60 mg, twice on the test day) or placebo, with the last dosing 2 h before the test in a double-blind, randomized, cross-over manner. On two separate study days, each subject drank the same brand and volume of alcoholic beverage (beer or Japanese saké), and bronchoconstriction was assessed as change in peak expiratory flow (PEF) over 120 min postchallenge. Inhalation challenges were performed with the same alcoholic beverage with which they had been orally challenged. The mean (SEM) percentage fall in PEF 15, 30, 45, 60, 90 and 120 min after the oral alcohol challenge was significantly reduced from 12.0 (3.1), 17.0 (1.7), 15.8 (2.3), 15.2 (3.4), 16.6 (4.8) and 14.7 (5.2)%, to 2.6 (1.8), 2.1 (1.6), 3.9 (1.2), 5.7 (2.2), 6.5 (2.6), 5.1 (1.6)%, respectively, by terfenadine. No significant bronchoconstriction was observed after the inhalation challenge. We conclude that the release of histamine makes a major contribution to alcoholic beverage-induced bronchoconstriction in Japanese asthmatic patients, and that histamine H1 antagonists may be effective in preventing alcoholic beverage-induced bronchoconstriction.

Adult↗

PubMed1993

[Effect of AS-35 aerosol on bronchoconstriction induced by specific antigens in macacus rhesus monkeys].

In a previous in vitro study, 9-[(4-acetyl-3-hydroxy-2-n-propylphenoxy) methyl]-3-(1H-tetrazol-5-yl)-4H- pyrido[1,2-a]pyrimidin-4-one (AS-35) was shown to have an inhibitory effect on antigen-induced mediator release and an antagonistic effect on leukotriene C4 and D4 receptors. In the present study, therefore, we investigated the effect of AS-35 aerosol on allergen-induced bronchoconstriction, using 6 female Macacus rhesus monkeys sensitized with DNP-Ascaris extracts (DNP-As). After treatment with an inactive placebo, inhalation challenge with DNP-As increased total lung resistance and decreased dynamic lung compliance dose-dependently 1 week after sensitization with DNP-As. Treatment with AS-35 aerosol, however, significantly inhibited allergen-induced bronchoconstriction dose-dependently 2 weeks after the sensitization. The inhibitory effect was about ten times more potent than that of DSCG. Because we confirmed that DNP-As evoked almost the same bronchoconstriction 1 and 2 weeks after sensitization and also that AS-35 did not inhibit histamine-induced bronchoconstriction at all, we inferred that AS-35 diminished allergen-induced bronchoconstriction by inhibiting allergen-induced mediator release from the cells in the airway.

Aerosols↗

PubMed1994

Inhibitory effect of aerosol administration of a sulfidopeptide leukotriene antagonist on bronchoconstriction induced by antigen inhalation in guinea pigs.

The effects of inhalation of the sulfidopeptide leukotriene antagonist AS-35 (9-[(4-Acetyl-3-hydroxy-2-n-propyl-phenoxy)methyl]-3-(1H- tetrazol-5-yl)-4H-pyrido [1,2-a]pyrimidin-4-one, CAS 108427-72-1) on bronchoconstriction induced by aerosol antigen, histamine, and leukotriene C4, D4 (LTC4, D4) were investigated in anesthetized and artificially ventilated guinea pigs. The increase in pressure at the airway opening (P(ao)) was measured as an index representing the grade of bronchial response. The bronchoconstriction induced by aerosol antigen was suppressed dose-dependently by pretreatment with inhaled AS-35 (0.1 mg and 1 mg) through a pressurized meter-dosed inhaler in the passively sensitized animals pretreated with diphenhydramine hydrochloride. But the histamine-induced bronchoconstriction was not altered by the pretreatment with AS-35 inhalation. On the other hand, LTC4- and LTD4-induced bronchoconstriction was inhibited by the pretreatment with aerosol AS-35 in a dose-dependent manner. The deposited dose of inhaled AS-35 in the peripheral airways was 3.5 micrograms and 6.5 micrograms when 0.1 mg and 1 mg of the drug was inhaled, respectively. These results suggest that sulfidopeptide leukotrienes (s-LTs) play an important role in the allergic bronchoconstriction in guinea pigs pretreated with antihistamine, and AS-35 inhalation may be beneficial in the treatment of asthma.

Administration, Inhalation↗

PubMed1993

Role of the complement system in antigen-induced bronchoconstriction and changes in blood pressure in the guinea pig.

Systemic anaphylaxis involves life-threatening bronchoconstriction and a serious hypotensive response often complicated by cardiac arrhythmias. The purpose of the present study was to determine whether complement system activation is essential to the bronchoconstriction and the changes in blood pressure seen in guinea pig models of anaphylaxis. The soluble complement receptor 1 (sCR1; BRL 55730) was used to inhibit activation of the classical and alternative pathways of complement in the guinea pig, and to determine whether this inhibition prevents bronchoconstriction and changes in blood pressure induced by i.v. antigen injection in guinea pigs that are either passively or actively sensitized to the antigen ovalbumin. sCR1 at 15 mg/kg did not affect significantly either the antigen-induced bronchoconstriction or the changes in blood pressure in a guinea pig passively sensitized with immunoglobulin G antibody to ovalbumin. However, it shortened the duration of the antigen-induced increase in blood pressure and inhibited the antigen-induced decrease in circulating platelets in an actively sensitized guinea pig. Continued studies using a cumulative dose of sCR1 of 105 mg/kg administered over a 24-hr period demonstrated that sCR1 attenuated the bronchoconstrictor response and the decrease in circulating platelets and prevented the hypotension induced by antigen in an actively sensitized guinea pig. At a cumulative dose of 105 mg/kg, sCR1 did not inhibit the bronchoconstrictor or blood pressure response to either histamine or bradykinin, indicating that its attenuation of cardiovascular and respiratory reactivity is specific for complement-related processes. The anaphylactic response was accompanied by complement activation as evidenced by cleavage of the C3 molecule. In the presence of sCR1, no C3 cleavage products were detectable in the plasma. Our studies demonstrate that complement activation is an essential step in the antigen-induced bronchoconstriction and the changes in blood pressure in an actively sensitized guinea pig model of anaphylaxis. Continued studies of the differing mechanisms and mediators of anaphylaxis are of importance, and the complement system clearly warrants consideration as a source of those mediators.

Animals↗

PubMed1995

[Mechanisms of hypertonic saline-induced bronchoconstriction in guinea pigs].

We examined whether inhalation of hypertonic saline can induce bronchoconstriction in guinea pigs, and also studied the mechanisms of this bronchoconstriction. Twenty-five male Hartley guinea pigs were divided into the following 5 groups: G-1, 0.9% saline inhalation; G-2. non-treatment and inhalation of hypertonic saline; G-3, capsaicin pretreatment and inhalation of hypertonic salines; G-4, ipratropium bromide pretreatment and inhalation of hypertonic saline; G-5, chlorpheniramine pretreatment and inhalation of hypertonic saline. RL and Cdyn were serially measured to assess bronchoconstriction, and the percent increase in RL from the value measured before inhalation of hypertonic saline (%RL) was analyzed. The maximum %RL was 9.2 +/- 3.8% in G-1, 90.6 +/- 6.6% in G-2, 11.2 +/- 5.7% in G-3, 9.0 +/- 6.0% in G-4, and 47.8 +/- 4.0% in G-5. The values in G-3 and G-4 were significantly lower than in G-2. We conclude that inhalation of hypertonic saline causes concentration dependent bronchoconstriction in guinea pigs and that both non-adrenergic non-cholinergic nerves and cholinergic nerves may play an important role in this bronchoconstriction.

Animals↗

PubMed1995

[The influence of misoprostol on post-aspirin bronchoconstriction in patients with aspirin sensitive asthma].

It is believed that aspirin (ASA) and other nonsteroidal antiinflammatory drugs elicit dysponea in ASA sensitive asthmatics by blocking the cyclooxygenase. It is unclear whether this bronchospasm is due to shunting of arachidonic acid into the lipooxygenase pathway or removal of cyclooxygenase product which prevent bronchospasm. Diminished tissue concentration of PGE may cause bronchoconstriction. PGE play also modulatory function to mast call decreasing the release of mediators of anaphylaxis. There are some evidences concerning the mast cell degranulation in postaspirin reaction in ASA sensitive asthmatics. The authors investigated the influence of synthetic analogue of PGE1--misoprostol (Cototec, Searle) on the postaspirin bronchoconstriction in seven ASA sensitive asthmatics aged 33-62. Aspirin threshold doses ranged from 10 to 150 mg. Postaspirin bronchoconstriction begun usually within 1-2 hrs after digestion of ASA and 200 micrograms were additionally given 2 h later. Seven days later misoprostol (400 micrograms) was administered together with previously determined dose of ASA. One the other day the bronchodilating effect of misoprostol alone was examined. In all but one patients we observed the protective influence of misoprostol on ASA induced bronchoconstriction. Max. fall in FEV1 in % after ASA in each of the patients was 40, 25, 24, 33, 47 and 54, and after ASA with misoprostol, respectively 10, 9, 4, (+8), 10, (+2) and 45. Misoprostol given together with ASA attenuated aspirin-induced bronchoconstriction reaching statistical significance at 3 and 3.5 h, and also diminished extrapulmonary symptoms. The authors discuss the possible mechanism of protective influence of misoprostol.

Adult↗

PubMed1997

The inhibitory effect of TMK688, a novel anti-allergic drug having both 5-lipoxygenase inhibitory activity and anti-histamine activity, against bronchoconstriction, leukotriene production and inflammatory cell infiltration in sensitized guinea pigs.

BACKGROUND: TMK688 is being developed as an anti-allergic drug having both 5-lipoxygenase inhibitory activity and anti-histamine activity. METHOD: We compared the inhibition of the late asthmatic responses by TMK688 with that by other anti-allergic agents in actively sensitized guinea pigs, and examined the relationship between 5-lipoxygenase inhibition and the late asthmatic responses. RESULTS: At 1-3.2 mg/kg, TMK688 inhibited the increases in respiratory resistance, leukotriene (LT) B4 and C4 production in the lungs and eosinophil infiltration into the alveoli during the late asthmatic response, whereas the effects tended to lessen at the dose of 10 mg/kg. These effects are thought to be caused by the 5-lipoxygenase inhibitory activity of TMK688 because Azelastine, an anti-allergic drug having potent antihistamine activity, exhibited no effect. ONO-1078, a peptide LT antagonist, inhibited the late-phase bronchoconstriction at a dose of 100 mg/kg p.o., but not the increase in the infiltration of inflammatory cells into the alveoli, suggesting that the late-phase bronchoconstriction is induced, in part, by peptide LTs, i.e. LT C4, D4 and E4 and that the inflammatory cell infiltration may be caused by LTB4. TMK688 inhibited the immediate bronchoconstriction dose-dependently, and the effect was significant at a dose of 10 mg/kg orally. Since Azelastine, Ketotifen and Oxatomide suppressed the bronchoconstriction at far lower doses than did TMK688, the inhibitory effect was mainly caused by its antihistamine activity. CONCLUSIONS: TMK688 appears to be a novel anti-allergic drug having inhibitory effects on both the bronchoconstriction and the infiltration of inflammatory cells during late asthmatic responses.

Animals↗

PubMed1997

Role of leukotrienes in post-allergic propranolol-induced bronchoconstriction in guinea-pigs.

BACKGROUND: Administration of propranolol can provoke bronchoconstriction only in asthmatic patients. Recently we developed an animal model for propranolol-induced bronchoconstriction (PIB). Our working hypothesis is that such bronchoconstriction may result from the inflammatory mediators released by an allergic reaction. OBJECTIVES: Our goal in this study was to determine which products of arachidonate 5-lipoxygenase pathway are involved in the PIB. METHODS: Propranolol at a concentration of 10 mg/mL was inhaled 20 min after antigen challenge in passively sensitized, anaesthetized and artificially ventilated guinea-pigs. Two different sulfidopeptide leukotriene (s-LT) antagonists, ICI198 615 in the doses of 0.03 and 0.3 mg/kg and vehicle and KCA757 in the doses of 1 and 5 mg/kg and vehicle, and a LTB4 antagonist ONO4057 in the doses of 1 and 10 mg/kg and vehicle were injected intravenously 15 min after antigen challenge. Effects of an anticholinergic agent atropine sulphate (5mg/kg) and an alpha-adrenergic blocker phentolamine (0.3 and 3 mg/kg) were examined in the same way. RESULTS: Bronchoconstriction occurred when 10 mg/mL of propranolol was inhaled 20 min after antigen challenge. Both ICI198 615 and KCA757 administered intravenously 15 min after antigen challenge reduced the PIB in a dose-dependent manner while ONO4057 did not alter the PIB. Atropine or phentolamine did not change the PIB. CONCLUSIONS: These results suggest that mediator mechanism, but not cholinergic or alpha-adrenergic nerve, is important in the PIB which developed after the allergic bronchoconstriction in our guinea-pig model and that s-LTs but not LTB4 have an important role in the pathophysiology of the PIB.

Adrenergic alpha-Antagonists↗

PubMed2000

Nedocromil sodium vs. sodium cromoglycate for preventing exercise-induced bronchoconstriction in asthmatics.

BACKGROUND: Nedocromil sodium and sodium cromoglycate inhaled shortly before exercise appear to reduce the severity of exercise-induced bronchoconstriction. There is some debate over which drug may be more effective. OBJECTIVES: The objective of this review was to compare the effects on post-exercise lung function between prophylactic doses of nedocromil sodium (NSG) and sodium cromoglycate (SCG) in persons diagnosed with exercise-induced bronchoconstriction. SEARCH STRATEGY: Randomized controlled trials were identified from the Cochrane Airways Review Group Asthma Register which compiles searches of CINAHL, EMBASE, MEDLINE and CENTRAL, plus hand searches for trials in 20 journals. Bibliographies of relevant studies and review articles were searched and primary authors, content experts and manufacturers of drugs were contacted for additional relevant studies. No language restrictions were applied. SELECTION CRITERIA: Randomized controlled trials comparing NCS to SCG in prophylactic treatment of exercise-induced bronchoconstriction were eligible. Studies were included if: the participants, aged 6 or over, had a confirmed diagnosis of asthma with exercise-induced bronchoconstriction, were subjected to an exercise challenge sufficient to trigger bronchoconstriction, and the measures of lung function were reported as either changes in forced expiratory volume in one second or peak expiratory flow rate. DATA COLLECTION AND ANALYSIS: Data extraction and methodological quality assessments were conducted independently by two reviewers using standard forms and validated assessment criteria. In some cases results were extrapolated from graphs. Results from similar studies were pooled and reported as the weighted mean difference (WMD) or odds ratio (OR) with 95% confidence intervals (CI) using the random effects model. MAIN RESULTS: Of the 92 citations retrieved from the original search, a total of 8 studies were included in this review (117 participants). No significant difference was noted between NCS and SCG with respect to the maximum percent decrease in FEV1 (WMD = -0.88; 95% CI: -4.50, 2.74), complete protection (i.e. maximum % fall FEV1 still =>10%); OR = 0.95; 95% CI: 0.50 to 1.8, clinical protection (i.e. < 50% improvement over placebo); OR = 0.71; 95% CI: 0.36 to 1.39; unpleasant taste (OR = 6.85; 95% CI: 0.77, 60.73), or sore throat (OR = 3.46; 95% CI: 0.32, 37.48). For these pooled comparisons, no statistically significant heterogeneity was identified. Subgroup analyses based on age, dosage of medications and timing of exercise post-inhalation were consistent with the overall pooled analyses. REVIEWER'S CONCLUSIONS: No significant differences were evident between the effect of NCS and SCG during the immediate post-exercise period in adults and children with EIB with regards to pulmonary function - specifically maximum percent decrease in FEV1, complete protection, clinical protection, or side effects.

Administration, Inhalation↗

PubMed1982

The action of disodium cromoglycate on allergen-induced bronchoconstriction.

The influence of DSCG administered to the upper and lower area of the air-conducting system on antigen-induced bronchoconstriction was studied in 34 dogs. In high doses DSCG administered to the upper airtract blocked bronchoconstriction and histamine release induced from the lower airways. Bronchoconstriction and histamine release originating from the upper airtract were not completely blocked by this kind of drug administration. Effects were differently strong in the individual animals. High doses of DSCG, administered to the lower airways, showed significant effect on bronchoconstriction originating from the lower airways. There was some yet nonsignificant effect on histamine release. Inhibition of respiratory activity without parallel inhibition of histamine release might suggest that plasma histamine concentration does not reflect the mode of action of DSCG in antigen-induced bronchoconstriction.

Animals↗

PubMed1990

Adenosine enhances antigen-induced bronchoconstriction and histamine release in rat isolated lungs.

The effects of adenosine and some of its analogues on bronchoconstriction and mediator release were studied in isolated lungs of actively sensitized rats. Adenosine (ADO) and its analogues R-phenyl-iso-propyl-adenosine (R-PIA) and N-ethyl-carboxamide-adenosine (NECA), enhanced antigen-induced bronchoconstriction in a dose-dependent manner. The enhancement of anaphylactic bronchoconstriction by adenosine and its analogues was accompanied by a rise in histamine release. The observed rank order of potency for adenosine and analogues (NECA greater than or equal to R-PIA greater than ADO) did not permit an unequivocal classification of the adenosine receptor involved. Dipyridamole and S-(p-nitrobenzyl-6-thioinosine) (NBTI), both inhibitors of adenosine uptake, had no inhibitory influence on the adenosine-induced enhancement of anaphylactic bronchoconstriction. Therefore, this enhancement was likely to be mediated through an extra-cellular receptor. Theophylline inhibited the enhancement of anaphylactic bronchoconstriction by adenosine in a concentration-dependent manner, without affecting preformed mediator release.

Adenosine↗

PubMed1984

Effect of histamine, acetylcholine and compound 48/80 on bronchoconstriction and release of eicosanoids in the dog.

The effects of Hi and ACH aerosol and of intravenous infusion of compound 48/80 on bronchoconstriction and plasma levels of Hi, TXB2, KH2PGF2 alpha and KH2PGE2 were investigated in 11 bastard dogs. Administration of Hi and ACH aerosol induced bronchoconstriction accompanied by an increase in the plasma levels of Hi and TXB2. No effect on the plasma levels of KH2PGF2 alpha and KH2PGE2 was detected. Release of endogenous Hi by compound 48/80 induced bronchoconstriction and significant increases in the plasma levels of TXB2 as well as of KH2PGF2 alpha and KH2PGE2. The effects of a second administration of Hi and ACH aerosols after compound 48/80 did not differ qualitatively from the effects of the first aerosol administration. However, quantitatively, the second Hi aerosol induced significantly less bronchoconstriction and TXB2 release. Similarly, effects of the second ACH aerosol tended to be decreased as compared to the first ACH aerosol, although the difference was not significant. The diminished effect of the agonists could be due to receptor desensibilization and/or release of adrenaline, which in turn decreases bronchoconstriction and eicosanoid release.

Acetylcholine↗