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Results for “Bronchoconstriction”

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At least 775 records · Page 43Linked to original sources

PubMed1994

Tosyl arginine methyl ester induces bronchoconstriction in rabbit bronchial tissues in vitro: a possible new mediator in asthma.

Tosyl arginine methyl ester induced bronchoconstriction in rabbit bronchial rings mounted in vitro with a calculated EC50 of 5.6 x 10(-5) M as compared with acetylcholine which induced sustainable constriction with an EC50 of 2.5 x 10(-6) M. Tosyl arginine methyl ester, however, had definite bronchoconstricting properties though less potent than acetylcholine. We concluded that our data support the hypothesis that tosyl arginine methyl ester could be a possible biochemical mediator of airway contraction.

Acetylcholine↗

PubMed1993

[A case of hypersensitivity pneumonitis induced by toluene diisocyanate presenting with transient bronchoconstriction].

A 50-year-old male spray paint worker was admitted with non-productive cough and dyspnea on exertion. Chest X-ray and chest CT showed diffuse interstitial shadows in the bilateral lung fields. After admission, the symptoms and chest X-ray findings improved over several days, and he was followed as an outpatient. He then developed nocturnal dyspnea with wheezing and dry cough every day. About two months later, chest X-ray showed more severe diffuse interstitial shadows which did not disappear after admission. Bronchoalveolar lavage and transbronchial lung biopsy revealed allergic exudative interstitial pneumonia, and he was treated with steroid therapy. Paint contains toluene diisocyanate, and challenge test to toluene diisocyanate was positive. In the early course, this case presented with bronchoconstriction; bronchial reversibility and bronchial hyperresponsiveness to methacholine were positive. Bronchoconstriction may cause worsening of respiratory symptoms in patients with hypersensitivity pneumonitis induced by isocyanates.

Alveolitis, Extrinsic Allergic↗

PubMed1993

[Influence of airway temperature and humidity of hyperventilation induced bronchoconstriction in rabbits].

It has been suggested that humidity and temperature of inspired air is important in determining the severity of hyperventilation induced bronchoconstriction (HIB). To investigate whether water loss or heat loss from airway plays more important role to induce HIB, we compared the effect of temperature and humidity of inspired air on HIB, in sensitized and non-sensitized rabbits. Inspired air containing 5% CO2 was conditioned to dry or humidified and to temperature of 9 degrees C or 25 degrees C during isocapnic hyperventilation. In sensitized rabbits, marked bronchoconstriction was observed when inspired air dry regardless of temperature. We conclude that 1) HIB is produced in sensitized rabbits and 2) humidity rather than temperature of inspired air is more important to induce HIB.

Animals↗

PubMed1993

Tracheal size is a determinant of the bronchoconstrictive response to inhaled methacholine.

We hypothesized that the size of the large airways is a determinant of bronchial responsiveness to inhaled methacholine. This was investigated by measuring the relationship of tracheal size and branching angle to the bronchoconstrictive response to methacholine, in 169 male construction insulators, aged 20-50 yrs, as part of a workforce-based, cross-sectional survey of respiratory health. Bronchial responsiveness was expressed as the concentration of methacholine, inhaled for 2 min of tidal breathing, which provoked a 15% fall in forced expiratory volume in one second (FEV1). Tracheal size was assessed from tracings of standard posteroanterior chest radiographs, at full inspiration. After accounting for the effect of airway calibre (FEV1/forced vital capacity (FVC)), age, height, and pack-years of cigarette smoking, on airways responsiveness, there was a significant association (p < 0.05) between tracheal length, diameter, or surface area and the degree of bronchoconstriction obtained by inhaling methacholine. The increase in airway responsiveness with decreasing tracheal size may reflect increased deposition of methacholine, secondary to smaller cross-sectional area and greater linear velocity of air in the trachea and main bronchi.

Adult↗

PubMed1996

Involvement of NO-ergic neural pathway in reflex tracheal dilatation during bronchoconstriction in guinea pigs.

The involvement of NOergic nerve in vagal reflex-mediated tracheal dilatation during bronchoconstriction was investigated using the guinea pig in vivo tracheo-bronchi separated preparation. Inhalation of 0.01% histamine to the bronchial site induced a biphasic, vagal reflex tracheal response, i.e., constriction followed by dilatation slightly after bronchial constriction. The reflex tracheal dilatation was inhibited by 49% by local treatment of the tracheal site with 1% propranolol. The residual dilatation in the presence of atropine and propranolol was significantly inhibited by 1% oxyhemoglobin or 1% carboxy-PTIO, NO scavengers. Cyclic GMP content in the tissue of the tracheal site during the reflex tracheal dilatation significantly increased. The increase in cyclic GMP was reduced by treatment of the tracheal site with 1% N omega-nitro-L-arginine methyl ester. These results support a hypothesis that reflex tracheal dilatation during bronchoconstriction may be mediated by not only adrenergic but also NOergic nerves in guinea pigs.

Administration, Inhalation↗

PubMedDate not supplied

Exercise-induced bronchoconstriction: elucidating the roles of leukotrienes and prostaglandins.

Exercise-induced bronchoconstriction (EIB) is prevalent among patients with symptomatic asthma, especially those with moderate-to-severe airway hyperresponsiveness. This phenomenon generally manifests within the first 3-5 minutes after exercise, during which the forced expiratory volume in 1 second (FEV1) markedly decreases. Usually, the FEV1 gradually returns to baseline within an hour. Exercise should not be avoided in patients with asthma, since improved physical fitness can reduce the minute ventilation associated with a given exercise work rate and, thereby, reduce the bronchoconstrictive response. The cysteinyl leukotrienes are becoming recognized as important mediators in EIB, and prostaglandins (released at least partially as a result of leukotriene stimulation) are gaining recognition for their protective effects. Thus, pharmacologic agents that either reduce leukotriene activity or enhance prostaglandin activity, or agents that do both, may enhance prophylaxis against EIB. Currently, beta-agonists and cromolyn sodium are the mainstays of prophylactic therapy for EIB.

Asthma, Exercise-Induced↗

PubMed1996

The role of the collagenous and elastic system fibers in modulating bronchoconstriction.

The distribution and conformational changes of the fibers of the collagenous and elastic systems in guinea pig airways after a contractile agonist challenge are described. We observed a distinct pattern of behavior within the mucosal fibers during bronchoconstriction. Part of the fibers of the two systems tend to follow the epithelial invaginations towards the airway lumen, while the remaining ones seem to be attached to the internal smooth muscle. These layers of fibers in the mucosa are interconnected to one another and to the adventitial network by slender fibers. We suggest that the configuration and behavior of these fibers during bronchoconstriction may contribute to airway reopening after the contractile stimulus has ceased. The possible role of this mechanism in the pathophysiology of human asthma is discussed.

Animals↗

PubMed1998

Effects of a 5-lipoxygenase inhibitor, ABT-761, on exercise-induced bronchoconstriction and urinary LTE4 in asthmatic patients.

The novel 5-lipoxygenase (5-LO) inhibitor, ABT-761, was investigated for its effect on exercise-induced bronchoconstriction in asthmatic subjects. The relationship between 5-LO inhibition and effects on the response of the airways to exercise was examined. In a double-blind, randomized, crossover clinical trial, 10 patients with mild to moderate persistent asthma (who exhibited a fall in forced expiratory volume in one second (FEV1) > or = 20% following standardized exercise challenge) received 200 mg ABT-761 or matched placebo, orally, 5 h prior to exercise on two study days, 7-10 days apart. Lung function, urinary leukotriene E4 (LTE4) and ex vivo calcium ionophore-stimulated LTB4 release in whole blood were measured prior to dosing, prior to exercise and at various time points up to 4 h post-exercise. The mean (SD) maximal percentage fall in FEV1 after exercise was 27.1 (12)% on placebo and 19.9 (10)% on ABT-761 days, respectively (p<0.05). Post-exercise fall in FEV1 was significantly attenuated at 5, 10, 15 and 30 min after exercise and the mean area under curve, representing the overall effect of exercise from 0-45 min post-challenge, was also significantly attenuated by ABT-761 (p<0.001). Ex vivo LTB4 release was inhibited by more than 80% throughout the 4 h post-exercise period, indicating that 5-LO was extensively inhibited at all time points. Urinary LTE4 in the post-exercise period was significantly lower after ABT-761 day than after placebo (40.1 (17.6) versus 89.8 (58.2) pg x mg creatinine(-1); p<0.05). Inhibition of LTB4 release in ABT-761-treated patients correlated positively with the attenuation of post-exercise FEV1 decline (r=0.711; p<0.05). We conclude that ABT-761 is effective in suppressing exercise-induced bronchoconstriction and that this protection is related quantitatively to the degree of 5-lipoxygenase inhibition.

Adult↗

PubMedDate not supplied

Respiratory muscle overloading and dyspnoea during bronchoconstriction in asthma: protective effects of fenoterol.

Whether, and to what extent, beta 2-agonists protect against respiratory muscle overloading and breathlessness during bronchoconstriction remains to be defined in patients with asthma. In a double blind placebo-controlled study, 100 micrograms of fenoterol were administered to six stable asthmatics before a bronchial provocation test, performed by inhaling doubling concentrations of histamine from a Devilbiss 646 nebulizer. We recorded breathing pattern (tidal volume VT, inspiratory time TI, total time of the respiratory cycle TTOT), inspiratory capacity (IC), dynamic pleural pressure swing (Pplsw), total lung resistance (RL) and FEV1. VT was expressed both in actual values and as % of IC. Changes in VT (%IC) during histamine inhalation reflected changes in dynamic end-inspiratory lung volume (EILV). Pplsw was expressed as % of maximal (the most negative in sign) pleural pressure, obtained under control conditions during a sniff manoeuvre (Pplsn). Pplsw (%Pplsn) is an index of inspiratory muscle effort. The test ended when the concentration of histamine which caused a decrease in FEV1 of > or = 40% post-saline was reached. Dyspnoea rating was scored by a modified Borg scale. At the ultimate degree of bronchoconstriction (UDB) with histamine: (i) decrease in FEV1 was similar after placebo and fenoterol, while increase in RL was lower after fenoterol (P < 0.005); (ii) VT(%IC) increased less after fenoterol (P < 0.027); (iii) increases in Pplsw (%Pplsn) was lower after fenoterol (P < 0.001); (iv) delta Borg (from saline) was lower (P < 0.01) after fenoterol; (v) differences in delta Borg, from placebo to fenoterol, related to concurrent changes in VT(%IC) (r2 = 0.67). In conclusion, at UDB 100 micrograms of fenoterol produced a beneficial effect on the degree of inspiratory muscle loading and breathlessness, an effect greater than it would be expected from measuring FEV1 alone.

Adrenergic beta-Agonists↗

PubMed1984

Bronchoconstriction: a component of the 'diving response' in man.

We have investigated the possibility that a bronchoconstriction accompanies the vagally-mediated bradycardia induced in man by immersion of the face in cold water. Forced expiratory flows (FEF) at 40% and 25% of vital capacity (VC) have been measured from partial flow-volume curves obtained during forced expirations starting at 70% VC. These were performed immediately after 15 s apnoea with or without face immersion, and compared with control expirations having the same volume history but without the preceding apnoea. Five of the 10 subjects showed evidence of a greater than 10% reduction in FEF, which averaged 17% (Fig. 2). Half the response was attributable to the apnoea alone and the other half, which was abolished by ipratropium, to cold face immersion (Fig. 3). This bronchoconstriction appears to be a new component of the 'diving response' in man, mediated, like the bradycardia, by vagal efferents.

Adult↗

PubMed1986

Formyl-methionyl-leucyl-phenylalanine causes bronchoconstriction in rabbits.

Formyl-methionyl-leucyl-phenylalanine (FMLP) is a synthetic acylated oligopeptide related to chemotactic peptides released by bacteria. In order to determine whether FMLP causes bronchoconstriction in vivo, we studied the effects of nebulized FMLP on lung resistance (RL) in the rabbit. In fourteen rabbits baseline RL was measured and than dimethylsulfoxide (DMSO) alone and 0.3, 1, 3 and 10 mg/ml FMLP in DMSO was nebulized and inhaled by the rabbits over periods of 2 min each. After each concentration the RL was re-measured and the results expressed as a % of the RL following DMSO alone. In 6 rabbits the response to serial nebulization of DMSO alone was 5.5 +/- 10.4% (mean +/- 2 SD). In 8 rabbits receiving FMLP there was a dose dependent increase in RL of 20% or greater whereas 6 rabbits failed to respond. Since there are known receptors for FMLP on neutrophils, 10 further rabbits were rendered neutropenic using nitrogen mustard and then studied as above. Eight of these rabbits failed to respond significantly to FMLP whereas 2 had a 20% or greater increase in RL. In each bronchial specimen from 6 additional rabbits FMLP failed to induce airway contraction in vitro. We conclude that FMLP causes a variable degree of bronchoconstriction in rabbits, that this response may, in part, be mediated via the neutrophil and is unlikely to be due to direct smooth muscle contraction.

Animals↗

PubMed1981

Leukotrienes C and D induce bronchoconstriction in man.

Pulmonary responses to aerosols of synthetic leukotrienes C and D were examined in two normal volunteers. The leukotrienes were equipotent and equieffective in producing moderate bronchoconstriction accompanied by coughing. Changes in FEV1 were slight, but changes in expiratory flow at low lung volumes were more notable. FPL 55712 abolished the cough response and partially inhibited the bronchoconstriction.

Adult↗

PubMed2001

Effects of non-bronchoconstrictive doses of inhaled propranolol on airway responsiveness to methacholine.

OBJECTIVES: The aim of this study was to evaluate the effects of non-bronchoconstrictive doses of propranolol on airway hyperresponsiveness to methacholine. METHODS: Double increasing concentrations (from 0.03 to 64 micrograms/ml) of inhaled propranolol were administered to a study population which included ten patients with mild asthma, ten rhinitics, and ten healthy control subjects. After the baseline bronchial responses to propranolol and methacholine, expressed as the cumulative provocative dose producing a 20% fall in forced expiratory volume in 1 s (PD20FEV1), were assessed, methacholine challenge was repeated after pretreatment with non-bronchoconstrictive doses of propranolol. RESULTS: The pharmacologically induced beta-blockade did not cause any effect in normal individuals, but it worsened airway responsiveness to methacholine in all asthmatics (geometric mean PD20 FEV1: 257 and 87 micrograms, respectively) and some rhinitics (geometric mean PD20 FEV1: 724 and 446 micrograms, respectively). CONCLUSION: Asthmatic patients were extremely sensitive to beta-blockers, whereas we observed a variable response to propranolol within the group of rhinitic subjects. This variability in the latter group is possibly because these individuals had different degrees of airway inflammation, increased parasympathetic activity, and beta-adrenoceptor dysfunction.

Administration, Inhalation↗

PubMed1985

Desensitization to PAF-induced bronchoconstriction and to activation of alveolar macrophages by repeated inhalations of PAF in the guinea pig.

Guinea-pig alveolar macrophages are activated in the presence of PAF-acether (PAF), as shown by O2.- production, suggesting that these cells, abundant in the lungs, are involved in PAF-induced bronchoconstriction. Alveolar macrophages collected after in vivo desensitization to the bronchoconstrictor effect of PAF became refractory to it in vitro, whereas the O2.- production in response to f-met-leu-phe persisted, although it was diminished suggesting a partial cross-desensitization. A similar desensitization to PAF was also observed in alveolar macrophages in vitro, demonstrating a stimulus-specific process. This study suggests that alveolar macrophages may be involved in bronchoconstriction induced by aerosol of PAF.

Aerosols↗

PubMed1984

Time course of exercise-induced bronchoconstriction in asthmatics exposed to sulfur dioxide.

Young adult asthmatic volunteers (N = 17) were exposed to 0.75 ppm sulfur dioxide (SO2) for 3-hr periods, exercising vigorously for the first 10 min and resting thereafter. Specific airway resistance (SRaw) and symptoms were recorded preexposure, immediately postexercise, and after 1, 2, and 3 hr of exposure. Symptoms and SRaw were significantly increased after exercise, relative to preexposure measurements. Group mean SRaw and symptom increases were no longer significant at 1 hr. In a few individuals, effects may have persisted for 2 hr or more. On separate occasions, comparable exposures were conducted, and forced expiratory spirometry was performed preexposure and postexercise, in addition to the other tests. Inclusion of spirometry did not significantly affect the other results. Spirometry and SRaw showed nearly equal significance in changes postexercise. Thus, in general, asthmatics' bronchoconstriction induced by exercise in SO2 seems to reverse quickly with rest, even if SO2 exposure continues. Spirometry may be useful for studying pollution-induced bronchoconstriction when SRaw measurements are impractical.

Adult↗

PubMed1989

Histamine H3-receptors modulate nonadrenergic noncholinergic neural bronchoconstriction in guinea-pig in vivo.

We have investigated whether the histamine H3-receptors influence nonadrenergic noncholinergic (NANC) bronchoconstriction in guinea-pig in vivo. Atropine, propranolol, mepyramine and cimetidine were administered to block the effects of beta-adrenoceptor-, acetylcholine, H1- and H2-receptor-mediated responses, respectively. Vagal stimulation evoked a NANC bronchoconstrictor response. The selective H3-agonist, alpha-methylhistamine (alpha-MeHA, 1-10 mg/kg i.v.) did not alter basal respiratory insufflation pressure, but reduced the NANC bronchoconstrictor response to vagal stimulation in dose-dependent manner (with a maximal inhibition of 46.0 +/- 10.3%; mean +/- S.E. at 10 mg/kg) (P less than 0.02). Histamine itself also had a significant inhibitory effect on NANC responses with H1- and H2-blockade. The alpha-adrenoceptor antagonist phentolamine had no effect on the inhibitory response produced by alpha-MeHA, but the H3-receptor antagonist thioperamide blocked the inhibitory effect of alpha-MeHA. alpha-MeHA had no inhibitory effect on bronchoconstriction induced by exogenous substance P (5-25 micrograms/kg i.v.). We conclude that H3-receptors inhibit the release of transmitter from NANC nerves and that H3-receptors might play a role in regulation of neurogenic inflammatory responses in the airways.

Animals↗

PubMed1987

Calcium dependency of massive postmortem bronchoconstriction in guinea pig lungs.

Calcium antagonists were employed to examine whether or not guinea pig's postmortem bronchoconstriction is calcium dependent. First, a group of 17 young (3-4-week-old) animals were divided in three subgroups: control, nifedipine, and 8-(N,N-diethylamino)-octyl-3,4,5-trimethoxybenzoate (TMB-8, an intracellular calcium antagonist). A second group of 12 mature (5-7-week-old) animals were divided into two subgroups: control and nifedipine. Baseline pressure-volume (P-V) curves were performed prior to cannulation of the pulmonary artery in the anesthetized, opened chested animal. The lungs of the animal were then perfused and P-V curves were obtained again at intervals for up to 60 min. Nifedipine (10(-6) M) or TMB-8 (5 X 10(-4) M) was added to the perfusate in experimental groups. A temporal decrease in inflation volume (IV, the lung volume between transpulmonary pressure of 0 and 30 cm H2O during inflation) was used as an indicator of bronchoconstriction. In control subgroups, the decrease in IV was significantly greater (P less than 0.05) in the young (29.5 +/- 12.9% baseline at 20 min) than in the mature animals (75.0 +/- 7.0% baseline at 20 min). Nifedipine significantly alleviated (P less than 0.05) the decrease in IV in young animals at 15-30 min (58.6 +/- 8.4% baseline at 20 min) while TMB-8 (90.6 +/- 2.1% baseline at 20 min) prevented the decrease even further. Nifedipine did not have a significant effect on IV in mature animals. These data suggest that the postmortem bronchospasm is much more severe in young animals and that this severe constriction is calcium dependent.

Age Factors↗

PubMed1982

Bronchoconstriction caused by Florida red tide toxins.

T17, a toxin purified from laboratory cultures of Florida's redtide organism, Ptychodiscus brevis (formerly Gymnodinium breve), produces bronchoconstriction in anesthetized artificially-ventilated guinea pigs. Bronchoconstriction, measured as a resistance to mechanical pulmonary inflation, was antagonized by atropine, but not by interruption of vagal nerve stimulation or diaphragm dissection.

Animals↗