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PubMed1997

Bronchoconstriction and eosinophil recruitment in guinea pig lungs after platelet activating factor administration.

Using a forced expiratory maneuver to measure flow volume loops, we evaluated the ability of platelet activating factor (PAF) to induce acute bronchospasm and in histological changes associated with bronchial asthma in guinea pigs. We determined both the dose-response curve and the time course of PAF-induced bronchoconstriction. Eight guinea pigs with weights ranging from 350 to 450 g were anesthetized, tracheotomized, and then paralyzed with gallamine. Baseline pulmonary function tests (PFT) were done. Different doses (25, 50, 100, 200, and 500 ng/kg) of PAF were injected through the jugular vein, and serial PFTs were done at 30 sec, 2, 5, and 20 min after each dose of PAF. Acetylcholine provocation testing was done following the 200 ng/kg dose of PAF. The PFTs included a forced expiratory maneuver, airway opening pressure (PaO), and total lung compliance (TLC). After all PFTs were completed, cell counts were done on fluid obtained from bronchoalveolar lavage (BAL) and the lungs were removed for histological study. Eight other guinea pigs were used as controls. The results showed that with increasing doses of PAF from 25 ng/kg to 200 ng/kg, all lung function parameters, including vital capacity, peak flow, MFEF 75%, MFEF 50%, MFEF 25%, and total lung compliance, gradually decreased. However, a further increase of the dose of PAF up to 500 ng/kg did not result in continued worsening of PFTs. The most severe bronchoconstriction occurred 30 sec after PAF was injected, and it gradually resolved thereafter. PAF injection also induced a severe inflammatory reaction of the airway and lung tissue, characterized by congestion, edema, inflammatory cell (especially lymphocytes and eosinophils) infiltration, and desquamation of bronchial epithelial cells. In conclusion, in the guinea pig model, PAF can induce acute reversible bronchospasm and bronchial hyperreactivity, as well as the typical histological changes of bronchial asthma.

Acetylcholine↗

PubMedDate not supplied

Cholinergic mechanisms and bronchoconstriction in guinea-pigs.

Seventy-four guinea-pigs have been actively sensitized against ovalbumin. The effects of bilateral cervical vagotomy and of cholinergic efferent blockade on the bronchoconstriction induced by inhaled acetylcholine, histamine or antigen have been quantified. Animals were curarized then tested during controlled ventilation to ensure constant conditions throughout the whole experiment by suppressing the post-vagotomy apneusis. Bronchial sensitivity was estimated by calculating the bronchoconstrictor dose-threshold provoking respiratory asynchronism. Corresponding variation of total lung resistance and dynamic compliance were also measured as indices of bronchial reactivity. The data obtained in 27 guinea-pigs indicated that the vagi section produced no significant effect on the direct bronchial response to histamine (P greater than 0.5), to acetylcholine (P greater than 0.1) or to antigen (P greater than 0.5). In 47 guinea-pigs, atropine at doses 5 and 10 times higher than the acetylcholine blocking one did not alter the direct bronchial response to histamine (P greater than 0.5). Higher doses induced a progressive decrease in bronchial sensitivity to antigen (.05 greater than P greater than .01) which could be related to the repetitive administration of the antigen. According to the present results, peripheral cholinergic mechanisms play no significant role in guinea-pigs neither in histamine nor in anaphylactic bronchoconstriction. Curarization has no influence on resting bronchial tone.

Acetylcholine↗

PubMed2000

Cutting edge: guinea pigs with a natural C3a-receptor defect exhibit decreased bronchoconstriction in allergic airway disease: evidence for an involvement of the C3a anaphylatoxin in the pathogenesis of asthma.

Asthma is a major cause of morbidity worldwide with prevalence and severity still increasing at an alarming pace. Hallmarks of this disease include early-phase bronchoconstriction with subsequent eosinophil infiltration, symptoms that may be mimicked in vivo by the complement-derived C3a anaphylatoxin, following its interaction with the single-copy C3aR. We analyzed the pathophysiological role of the C3a anaphylatoxin in a model of experimental OVA-induced allergic asthma, using an inbred guinea pig strain phenotypically unresponsive to C3a. Molecular analysis of this defect revealed a point mutation within the coding region of the C3aR that creates a stop codon, thereby effectively inactivating gene function. When challenged by OVA inhalation, sensitized animals of this strain exhibited a bronchoconstriction decreased by approximately 30% in comparison to the corresponding wild-type strain. These data suggest an important role of C3a in the pathogenesis of asthma and define a novel target for drug intervention strategies.

Administration, Inhalation↗

PubMed2002

Early phase bronchoconstriction in the mouse requires allergen-specific IgG.

Allergen provocation of allergic asthma patients is often characterized by an initial period of bronchoconstriction, or early phase reaction (EPR), that leads to maximal airway narrowing within 15-30 min, followed by a recovery period returning airway function to baseline within 1-2 h. In this study, we used a defined OVA provocation model and mice deficient for specific leukocyte populations to investigate the cellular/molecular origins of the EPR. OVA-sensitized/challenged wild-type (C57BL/6J) mice displayed an EPR following OVA provocation. However, this response was absent in gene knockout animals deficient of either B or T cells. Moreover, transfer of OVA-specific IgG, but not IgE, before the OVA provocation, was capable of inducing the EPR in both strains of lymphocyte-deficient mice. Interestingly, an EPR was also observed in sensitized/challenged mast cell-deficient mice following an OVA provocation. These data show that the EPR in the mouse is an immunologically based pathophysiological response that requires allergen-specific IgG but occurs independent of mast cell activities. Thus, in the mouse the initial period of bronchoconstriction following allergen exposure may involve neither mast cells nor IgE-mediated events.

Administration, Inhalation↗

PubMed2000

Laryngospasm and paradoxical bronchoconstriction after repeated doses of beta 2-agonists containing edetate disodium.

A 22-year-old woman with mild intermittent asthma, who had no previous history of an adverse reaction to an albuterol metered-dose inhaler, developed paradoxical bronchoconstriction after inhalation of the fourth dose of an albuterol nebulizer solution. She experienced the same symptoms and laryngospasm with repeated inhalations of albuterol and metaproterenol nebulizer solutions that contained edetate disodium. Each episode responded to racemic and subcutaneously administered epinephrine. To our knowledge, this is the first report of paradoxical bronchoconstriction and laryngospasm due to repeated doses of beta 2-agonist solutions with edetate disodium.

Administration, Inhalation↗

PubMed1998

[Effect of adrenomedullin on bronchoconstriction responses induced by histamine].

OBJECTIVE: To observe the effect of synthetic human adrenomedullin (AM) on anesthetized guinea pigs bronchoconstriction induced by histamine. METHOD: The guinea pigs were divided into saline group; isoproterenol groups at the dosages of 0.03 microgram/kg, 0.3 microgram/kg, 3 micrograms/kg and 30 micrograms/kg; adrenomedullin groups at the dosages of 0.02 microgram/kg, 0.2 microgram/kg, 2 micrograms/kg and 20 micrograms/kg. There were seven guinea pigs a group. Guinea pigs were anesthetized by sodium pentobarbital, normal saline group, isoproterenol and adrenomedullin at different dose i.v., while histamine (10(-4) mol/L) were vasolated and delivered into the airway. Body plethysmogroph was used to measure airway resistance and lung compliance. RESULT: The increment of airway resistance and decrement of lung compliance induced by histamine were inhibited significantly by isoproterenol at the dosages of 0.3 microgram/kg, 3 micrograms/kg and 30 micrograms/kg (P < 0.05). The increase of airway resistance was inhibited significantly by adrenomedullin at the dosages of 2 micrograms/kg and 20 micrograms/kg (P < 0.05). The decrease of lung compliance induced by histamine was inhibited significantly by adrenomedullin at 0.2 microgram/kg, 2 micrograms/kg and 20 micrograms/kg (P < 0.05). CONCLUSION: Adrenomedullin inhibited the bronchoconstriction induced by histamine significantly.

Adrenomedullin↗

PubMed2001

Controversies and challenges of exercise-induced bronchoconstriction and their implications for children.

The association of exercise with hyperresponsiveness and bronchoconstriction of the airways has been well-recognized. Exercise may be the sole trigger or one of many triggers in patients with asthma. Although it is clear that asthma and the symptoms brought about by exercise are closely intertwined, the pathophysiology underlying this process is not well-understood. Recent studies on the epidemiology of the disease have provided insights into the processes leading to exercise-induced bronchoconstriction, with particular significance for children with asthma.

Adolescent↗

PubMed2000

Effects of endothelin B receptor antagonists, BQ788 and ET-1(11-21) fragment on the bronchoconstriction elicited by isocapnic hyperpnea in guinea pigs.

OBJECTIVE: To explore the role of endothelin (ET) in the pathogenesis of exercise-induced asthma (EIA), we investigated the effects of ETB receptor antagonists, ET-1(11-21) fragment and N-cis-2, 6-dimethylpiperidinocardonyl-L-gamma-methylleucyl-D-1-methoxycarbonyl tryptophanyl-D-norleucine (BQ788) on bronchoconstriction elicited by isocapnic hyperpnea in guinea pigs. METHODS: Eighteen pathogen-free Hartley guinea pigs were randomly divided into three groups. A: normal saline (NS) inhalation control group (n = 6), B: BQ788 group (n = 6), and C: ET-1(11-21) fragment group (n = 6). Guinea pigs were anesthetized with pentobarbital sodium. After measuring the basal value of lung resistance (RL) and dynamic compliance of the respiratory system (Cdyn), NS (0.96 ml), BQ788 (9 nmol) and ET-1(11-21) fragment (9 nmol) were inhaled. A rodent respirator with a dry 5% CO(2)-95% O2 mixture at room temperature provided mechanical ventilation (VT8 ml/animal, 100 breaths/min) for 5 min. RL and Cdyn of the 3 groups were measured again after isocapnic hyperpnea challenge. RESULTS: In the control group, isocapnic hyperpnea of dry gas elicited a marked increase in RL and decrease in Cdyn. RL and Cdyn of the guinea pigs from BQ788 group and ET-1(11-21) fragment group did not change significantly. CONCLUSION: It was demonstrated that selective ETB receptor antagonists, ET-1(11-21) fragment and BQ788, inhibited the bronchoconstriction induced by isocapnic hyperpnea in guinea pigs. The data showed that ETs are potent constrictors of guinea pig airway smooth muscle via a direct effect on ET receptors. It was suggested that ET receptor antagonists, especially ETB receptor antagonist, might be beneficial in preventing EIA.

Airway Resistance↗

PubMed2003

[Effect of fexofenadine--selective antagonist of histamine receptor (H1) on histamine-induced bronchoconstriction].

The aim of the study was to evaluate the effect of single and repeated fexofenadine (120 mg/day) doses on histamine-induced bronchoconstriction. Sixteen patients with mild, stabile asthma were examined. Bronchial reactivity was estimated as histamine dose (in mg/ml) causing a 20% FEV1 fall. A significant blockade of histamine H1 receptors in the airways was observed from the 1st to the 3rd day of the study. In all patients treated with fexofenadine, histamine in 16 mg/ml dose failed to induce bronchoconstriction. After another three days without fexofenadine, bronchial responsiveness returned to the initial value. The study points out that fexofenadine blocks H1 receptors in the bronchial tree.

Adult↗

PubMed1992

[The inhibitory effects of anti-asthmatic agents on ethanol-induced bronchoconstriction in Japanese asthmatic patients].

Asthmatic symptoms are worsened after drinking small amounts of alcoholic beverages in Japanese asthmatic patients. Our previous results showed that the ingestion of pure ethanol caused a fall in FEV1.0 in about half of the Japanese asthmatics we studied. We studied the inhibitory effects of pretreatment with three kinds of anti-asthmatic agents on ethanol-induced bronchoconstriction in six Japanese asthmatic patients. We tested oral cyproheptadine hydrochloride (8 mg), which is an anti histamine agent, inhaled disodium cromoglycate (2 mg), which has an inhibitory effect on the release of chemical mediators from mast cells, and inhaled atropine sulfate (3 mg), which is an anti-cholinergic agent. Pretreatment with cyproheptadine significantly inhibited the fall in FEV1.0 120 minutes after ethanol challenge (p less than 0.05). Inhaled DSCG had significant inhibitory effects on the fall in FEV1.0 15 and 30 minutes after ethanol challenge (p less than 0.05). Inhaled atropine had no inhibitory effect. These results suggest that histamine, released from mast cells, plays an important role in ethanol induced bronchoconstriction in Japanese asthmatic patients.

Adult↗

PubMed1992

Protective effects of inhaled ipratropium bromide on bronchoconstriction induced by adenosine and methacholine in asthma.

Although adenosine-induced bronchoconstriction is mainly due to mast cell mediator release, vagal reflexes have also been implicated in this response. We have investigated the effect of a specific muscarinic-receptor antagonist, ipratropium bromide, on methacholine- and adenosine-induced bronchoconstriction in a randomized, placebo-controlled, double-blind study of 12 asthmatic subjects. Airway response was evaluated as forced expiratory volume in one second (FEV1). Inhaled ipratropium bromide (40 micrograms), administered 20 min prior to bronchoprovocation, increased the provocation dose of inhaled methacholine and adenosine required to reduce FEV1 by 20% from baseline (PD20) from 0.11 to 0.79 mg (p less than 0.01) and from 0.57 to 1.27 mg (p less than 0.01), respectively. The mean baseline FEV1 values after administration of ipratropium bromide were significantly higher than after placebo administration (p less than 0.05). However, there was no correlation between the degree of bronchodilatation and dose-ratios for methacholine and adenosine. The findings of the present study implicate vagal reflexes in the bronchospastic response induced by inhaled adenosine in asthma.

Adenosine↗

PubMed2004

[Tiotropium as a controller of bronchoconstriction].

Cholinergic nerve fibres arise in the nucleus ambiguus and the dorsal motor nucleus of the vagus nerve in the brainstem. They travel down as the vagus nerve to parasympathetic ganglia placed in the walls of the airways. From these ganglia, short postganglionic fibres innervate airway smooth muscle and the submucosal glands in the lung. Activation of vagal nerve releases acetylcholine at the neuroeffector junctions, where it binds to postsynaptic receptors, resulting in bronchoconstrictions. The resting bronchomotor tone in normal airways has a cholinergic component mediated via muscarinic cholinergic receptors. The human airways have five subtypes of muscarinic cholinergic receptors: the M1 and M3 mediate bronchoconstriction and stimulation of mucus secretion, while M2 control the release of acetylcholine from M1 and M3 receptors through a negative-feedback mechanism. Anticholinergic bronchodilators act by blocking muscarinic receptors. Tiotropium bromide is cutting age anticholinergic bronchodilator. It dissociates more slowly from M1 and M3 than from M2 receptors and subsequently has a long and safety duration of action. In COPD patients tiotropium comparing to placebo, ipratropium and long acting beta agonists significantly improves lung function. It is an effective bronchodilator that reduces dyspnea, COPD exacerbations frequency and improves health status. This suggests that tiotropium will make an important contribution to chronic pulmonary disease therapy.

Bronchi↗

PubMed1991

Effect of salbutamol on dry air- and acetylcholine-induced bronchoconstriction in the canine lung periphery.

We examined the effect of salbutamol on dry airflow-induced bronchoconstriction (AIB) and acetylcholine-induced bronchoconstriction (Ach-IB) in the canine lung periphery using a wedged bronchoscope technique. Collateral system resistance (Rcs) and airway wall temperature (Taw) were monitored in a peripheral lung segment before, during and after airflow challenge. Rcs before and after aerosolized acetylcholine was recorded in a contralateral lung segment. Intravenous salbutamol (2.5 micrograms.kg-1) significantly attenuated the peak fall in Taw during airflow challenge and the peak rise in Rcs following challenge. Intravenous salbutamol attenuated Ach-IB to a similar degree. Significant systemic effects were recorded following i.v. salbutamol. In contrast, aerosolized salbutamol (50 micrograms) minimally decreased the fall in Taw during airflow challenge, while virtually eliminating AIB. The same dose of aerosolized salbutamol only partially attenuated Ach-IB. Aerosolized salbutamol did not affect mean arterial pressure or heart rate. Intravenous salbutamol may in part inhibit AIB by increasing pulmonary blood flow, secondary to its systemic circulatory effects, and decrease heat and water loss during airflow challenge. In contrast, aerosolized salbutamol abolished AIB, while only minimally effecting airway cooling. These data suggest that AIB is a result of mediator release and/or smooth muscle contraction.

Acetylcholine↗

PubMed1991

Influence of water content of inspired air during and after exercise on induced bronchoconstriction.

This study looked at the influence of inspired air water content on exercise-induced bronchospasm (EIB). On separate days, 12 mild asthmatics (4M, 8F), aged 18-39 yrs (mean: 27 yrs), performed four six minute steady-state exercises on ergometer at 80% of their maximum workload. Exercises were randomized to the following inspired air conditions: dry air (0% relative humidity (RH] during exercise followed by dry (DD) or humid air (100% RH) (DH) after exercise, humid air during exercise followed by dry (HD) or humid air (HH). Room temperature was kept constant (22 +/- 1 degree C) at all visits. Forced expiratory volume in one second (FEV1) was measured before and every 5 min for 25 min after exercise. Ventilation (VE) was not significantly different whether the exercise was done under dry or humid air. There was a residual bronchodilatation at the end of exercises performed in humid air, while at this time FEV1 was already lower than baseline when exercise was done in dry air conditions. The maximal fall in FEV1(%) following exercise was significantly greater after those performed in dry air: DD (29 +/- 5.6%) and DH (30 +/- 5.8%) than in humid air: HD (12 +/- 4.9%) and HH (20 +/- 4.9%) (p less than 0.05). The time-course of recovery from bronchoconstriction was significantly improved when inhaling dry air after exercise. However, the difference found in the maximal % fall in FEV1 after exercise when recovery was in dry compared to humid air did not achieve statistical significance. In conclusion, EIB is influenced by the changes in water content during and after exercise. Bronchoconstriction following exercise is minimal if exercise is done in humid air and recovery in dry air, and maximal if the exercise is performed in dry air and recovery in humid air.

Adolescent↗

PubMed1991

Influence of lung volume on histamine-induced bronchoconstriction in guinea-pigs.

The influence of lung volume on bronchopulmonary reactivity was investigated in 4 groups of 14 anaesthetized paralysed mechanically ventilated guinea-pigs: animals of group 1 served as control; in animals of group 2, the parasympathetic nervous system was blockaded with atropine; animals of group 3 were submitted to a bilateral cervical vagotomy; animals of group 4 were both vagotomized and pretreated with atropine. In each group, the animals were randomly divided into 2 subgroups: one was ventilated at zero end-expiratory pressure (ZEEP), the other with 0.2 kPa positive end-expiratory pressure (PEEP) resulting in a mean increase in lung volume of about 1 ml. Bronchopulmonary response to infused histamine was assessed by the respiratory conductance and compliance values measured during bronchoconstriction (respectively HGrs and HCrs). In the control group, animals exposed to PEEP were found significantly less reactive than those ventilated at ZEEP. In groups 2, 3 and 4, this difference was significantly reduced for HGrs and even abolished for HCrs. These results demonstrate that the effect of lung volume on moderate histamine-induced bronchoconstriction in guinea-pigs is not purely mechanical, but is partly vagally mediated. They also suggest that this vagally mediated inhibitory influence results from involvement of central reflexes evoked by stretch receptor stimulation.

Animals↗

PubMed1995

[Effects of a beta 2-agonist, sodium cromoglycate, and an anticholinergic agent on hyperventilation-induced bronchoconstriction in sensitized rabbits].

Hyperventilation can induce bronchoconstriction in ovalbumin-sensitized rabbits. To investigate the roles of the beta-receptor parasympathetic nervous system and of chemical mediators in hyperventilation-induced bronchoconstriction (HIB), the effects of a beta 2-agonist, of sodium cromoglycate, and of an anticholinergic agent on HIB were studied. Rabbits were divided to four groups and treated as follows. Group 1: Control (n = 7, 0.9% saline); Group 2: Procaterol (n = 4, 50 micrograms/l); Group 3: Sodium cromoglycate (n = 4, 10 mg/ml); and Group 4: Ipratropium bromide (n = 6, 1 mg/ml). Each drug was inhaled for 1 min via an ultrasonic nebulizer. Then, for the eucapnic hyperventilation challenge, sensitized rabbits were mechanically hyperventilated for 15 min (120 breaths/min, tidal volume = 7 ml/kg) with dry air containing 5% CO2 at room temperature. Total lung resistance and dynamic compliance were measured before, and 0, 5, 15, and 30 min after hyperventilation. The mean percent change in resistance measured 5 min after the hyperventilation was +49% in group 1, -6% in group 2, +23% in group 3, and +1% in group 4. The changes in groups 2 and 4 were significantly less than in group 1 (p < 0.05). In conclusion, HIB is mainly caused by bronchial smooth muscle constriction, and chemical mediators and the parasympathetic nervous system may play important roles in the development of HIB in sensitized rabbits.

Acetylcholine↗

PubMed1995

Effect of ipratropium bromide and/or sodium cromoglycate pretreatment on water-induced bronchoconstriction in asthma.

The mechanisms underlying water-induced bronchoconstriction are still not fully understood. Cholinergic reflexes and mast cell mediator release are currently believed to play an important pathogenetic role. In order to evaluate the relative contribution of each of these mechanisms, we studied the effect of ipratropium bromide (80 micrograms), a muscarinic antagonist, and sodium cromoglycate (20 mg), an inhibitor of mast cell mediator release, administered alone and in combination, in the prevention of bronchospasm induced by ultrasonic mist of distilled water (UMDW). Fifteen patients with documented atopic asthma and hyperresponsiveness to distilled water were selected for this randomized, placebo-controlled, double-blind study. Airway responses to pharmachological agents and bronchial challenge were measured by change in specific airways conductance (sGaw). Sodium cromoglycate had no effect on bronchial calibre, whilst ipratropium bromide and the combination of the two drugs produced a significant bronchodilation 30, 60 and 90 min after treatments. The maximal increase in sGaw (mean % +/- SD) was observed at 90 min: 63 +/- 28% and 58 +/- 22% after ipratropium bromide and the combined drugs respectively. UMDW (2, 4, 8, 16 ml water) caused a -36 +/- 19%, -42 +/- 19%, -49 +/- 18%, -56 +/- 15% mean % +/- SD fall in sGaw after placebo. Pretreatment with sodium cromoglycate abolished the bronchoconstriction to 2 ml (fall sGaw -5 +/- 23% NS) and significantly reduced the effect of 4 (-15 +/- 22%), 8 (-21 +/- 20%) and 16 ml (-24 +/- 18%) water.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Inhalation↗

PubMed1994

Dose-related protection against histamine-induced bronchoconstriction by inhaled salmeterol.

A double-blind crossover study was carried out in 8 subjects to compare the effect of inhaled salmeterol 12.5, 50 and 100 micrograms with inhaled salbutamol 200 micrograms on resting lung function and on bronchoconstriction in response to inhaled histamine up to 12 hours following each treatment. Changes in resting lung function were measured using forced expiratory volume in one second (FEV1) and flow at 70% of vital capacity taken from partial expiratory flow volume curves (pEFR70). The concentrations of histamine which produced a 15% fall in FEV1 (PC15) and a 40% fall in pEFR70 (PC40) were also measured. The peak bronchodilator effect after salmeterol 50 and 100 micrograms was similar in magnitude to salbutamol 200 micrograms. Salmeterol produced dose-related changes in lung function and protection against histamine-induced bronchoconstriction. The duration of the effect of salmeterol (50 and 100 micrograms) was longer than that for salbutamol (200 micrograms). Although pEFR70 is a more sensitive measure of lung function there was no greater separation between different doses of salmeterol than with FEV1. Both salmeterol and salbutamol were well tolerated.

Administration, Inhalation↗