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PubMed1976

The effect of thymoxamine and cromolyn sodium on postexercise bronchoconstriction in asthma.

Of the 22 patients with extrinsic bronchial asthma, 13 patients developed post-exercise bronchoconstriction after treadmill exercise, whereas in 9 patients treadmill exercise had no effect on the ventilatory capacity. No statistical difference in the resting lung volumes and CO transfer factor was found between the two groups. A significant inhibition of postexercise bronchoconstriction was observed in 12 of 13 patients following thymoxamine or cromolyn sodium inhalation. Inhibition of postexercise bronchoconstriction by alpha blockade with thymoxamine suggests that increased alpha adrenergic activity in the presence of diminished beta receptor responsiveness to catecholamines, norepinephrine released during exercise could have a marked alpha agonistic effect giving rise to bronchoconstriction. It has been suggested that cromolyn sodium has a cyclic phosphodiesterase inhibiting action. This might increase levels of AMP and restore the beta receptor responsiveness to catecholamines.

Airway Obstruction↗

PubMed1985

Bronchodilatation and inhibition of allergen-induced bronchoconstriction by circulating epinephrine in asthmatic subjects.

The influence of circulating epinephrine on basal bronchial tone and its ability to counteract the bronchial response to specific allergen challenge was investigated in eight patients with extrinsic seasonal asthma. A pretrial bronchial allergen challenge was positive for birch or timothy pollen. The patients were free from all medication at least 1 wk before experiments. On two separate occasions placebo (saline) or epinephrine (0.25 and 0.50 nmol X kg-1 X min-1) were infused. Epinephrine caused dose-dependent increases in end expiratory flow rates but did not influence peak expiratory flow rates or specific airway conductance, indicating dilatation of predominantly smaller airways. During placebo infusions allergen provocation induced clear-cut bronchoconstriction but no increase in circulating epinephrine levels. Elevation of circulating epinephrine (to 5 to 6 nmol/L in venous plasma) counteracted the allergen-induced bronchoconstriction. During epinephrine infusions all patients tolerated higher allergen doses than during placebo infusions. When the allergen dose was increased sufficiently to cause bronchoconstriction also during epinephrine infusions, the bronchoconstriction observed was similar in terms of changes in lung function parameters but less responsive to treatment with a high dose of the beta-2-agonist, salbutamol. This may have therapeutic implications since protection offered by treatment with, e.g. beta 2-agonists, may lead to exposure to higher allergen doses and similarly aggravated asthmatic reactions when they do occur despite this treatment.

Adult↗

PubMed1987

A new method of inhalation challenge with propranolol: comparison with methacholine-induced bronchoconstriction and role of vagal nerve activity.

To establish a safe procedure for examining propranolol-induced bronchoconstriction, we have developed a new method for performing inhalation challenge with propranolol. Monitoring respiratory resistance during tidal breathing with continuous inhalation of propranolol in 1.5-fold increasing concentrations from 0.78 to 30 mg/ml for 1 minute at each concentration, we tested 43 subjects with stable asthma and 10 normal subjects. We also compared bronchial responsiveness with responsiveness to inhaled methacholine on separate days. In addition, to determine the role of vagal nerve activity in propranolol-induced bronchoconstriction, we studied the effect of atropine. Inhaled propranolol caused dose-related bronchoconstriction in all subjects with asthma but not in normal subjects. None of the subjects suffered severe asthmatic attack during the test, which was performed in 15 minutes or less. The minimum cumulative dose of methacholine and of propranolol, at the point where respiratory conductance began to decrease, was not significantly correlated. Increased respiratory resistance was reversed by atropine in 70% of the subjects with asthma with marked individual differences. These data suggest that, although in most subjects with asthma, vagal nerve activity contributes in varying degree to bronchoconstriction, other constricting factors may contribute in the remaining subjects. It is also suggested that the mechanism of bronchial response to propranolol differs from that of the nonspecific airway reactivity estimated by methacholine challenge.

Adolescent↗

PubMed1988

Therapeutic range cromolyn dose-response inhibition and complete obliteration of SO2-induced bronchoconstriction in atopic adolescents.

Eight atopic adolescent subjects with exercise-induced bronchospasm were studied to determine whether cromolyn sodium could inhibit or block sulfur dioxide (SO2)-induced bronchoconstriction. Cromolyn or placebo were administered by turboinhaler 20 minutes before 10 minutes of SO2 exposure at 1.0 ppm during continuous moderate exercise on a treadmill. The exercise level that was chosen did not in itself produce bronchoconstriction. The cromolyn doses were 0 (placebo), 20, 40, and 60 mg. Pulmonary functions (FEV1, and total respiratory resistance) were measured before and after drug administration and after exposure. SO2 exposure after placebo produced significant bronchoconstriction. Pretreatment with 20 mg of cromolyn did not change the SO2 response, 40 mg significantly inhibited the response, and 60 mg completely abolished the pulmonary function changes. These results demonstrate for the first time a dose-response inhibition of SO2-induced bronchoconstriction in atopic subjects within a clinically acceptable dosage range and complete obliteration of SO2 sensitivity in this group with 60 mg of cromolyn pretreatment.

Adolescent↗

PubMed1985

A lung perfusion technique for the detection of antigenic intrapulmonary bronchoconstriction and its mediation.

A guinea pig intraluminal perfusion model was used to assess the effects of antigen challenge of airway reactivity and its pharmacologic modulation. Increases in airway perfusion pressure, following antigen provocation, could be reproduced 60 min later without significant modification of the response. We found no change in lung volume nor observed tissue edema following antigen provocation, and suggest that rises in perfusion pressure are due to decreases in airway caliber. Pharmacologically, the antihistamines, mepyramine and chlorpheniramine, and the antiallergic agent, disodium cromoglygate (DSCG), failed to inhibit antigenic bronchoconstriction. Indeed, mepyramine produced some potentiation of allergic bronchospasm. Compounds reported to inhibit 5-lipoxygenase (phenidone, benoxaprofen, and noradihydroguiaretic acid (NDGA)) or antagonize SRS-A (FPL 55712), produced inhibition of antigen-induced bronchoconstriction. The cyclooxygenase inhibitor, indomethacin, produced biphasic modulation of antigenic bronchoconstriction, potentiation at low doses, and inhibition at high concentrations. Overall, drug-induced modulation of allergic bronchoconstriction suggests that this model more closely resembles the antigenic reactions observed in the parenchymal strip preparation than in the trachea.

Animals↗

PubMed1987

The effects of albuterol on sulfur dioxide-induced bronchoconstriction in allergic adolescents.

Ten allergic subjects with exercise-induced bronchospasm were studied to determine whether albuterol could prevent sulfur dioxide (SO2)-induced bronchoconstriction. Albuterol or placebo (180 micrograms) were administered by metered-dose inhaler 20 minutes before a 10-minute exposure to SO2 or clean air during moderate exercise on a treadmill at an exercise level that by itself did not produce exercise-induced bronchospasm. Pulmonary functions (FEV1 and total respiratory resistance [RT]) were measured before the drug, after the drug, and after exposure to SO2 or clean air. Albuterol treatment produced significant bronchodilation and also prevented SO2-induced bronchoconstriction. Following SO2 inhalation after placebo, FEV1 decreased 15% (p less than 0.02) and RT increased 50% (p less than 0.03). Following SO2 inhalation after albuterol treatment, neither FEV1 or RT changed significantly. We conclude that albuterol, a beta 2-agonist, inhibits SO2-induced bronchoconstriction. This result suggests that the adrenergic nervous system or mast cell degranulation are involved in SO2-induced bronchoconstriction.

Adolescent↗

PubMedDate not supplied

Early and late phase bronchoconstrictions in conscious sensitized guinea-pigs after macro- and microshock inhalation of allergen and associated airway accumulation of leukocytes.

Guinea-pigs were sensitized by i.p. injection of 10 micrograms OA and 100 mg aluminium hydroxide in 1 ml normal saline. Fourteen to twenty-one days after sensitization, animals were exposed to macroshock (1% OA for 2 min) or microshock (0.01% for 60 min) inhalation challenges with OA. Animals were protected against fatal anaphylaxis in the case of macroshocks with mepyramine (30mg/kg i.p.) 30 min before exposure. Specific airway conductance (sGaw) was measured in conscious animals by whole body plethysmography at intervals up to 72 h after challenge. An early phase bronchoconstriction peaked significantly (P < 0.05) at 15 min after both macroshock and microshock OA exposures, with maximum falls in sGaw of 70.8 +/- 3.8 and -40.0 +/- 5.9%, respectively. These had resolved after 5 h. A late phase bronchoconstriction peaked variably between 17 and 24 h: the mean peak falls in sGaw after the macro- and microshock challenges were significantly different from baseline (P < 0.05), at -21.6 +/- 3.7 and -38.0 +/- 3.9%, respectively. Control exposures of OA-sensitized guinea-pigs to saline for either 2 or 60 min, in place of OA, produced no significant variation in sGaw values over the predicted early and late phases. Bronchoalveolar lavage (BAL) performed at 5 or 24 h after OA challenge revealed significant increases in total cell numbers (P < 0.05) at 5 and 24 h after the OA macroshock challenge and at 24 h after the microshock, compared with saline challenges. Differential cell counts showed a significant (P < 0.05) increase in the proportion of neutrophils at 5 h and of neutrophils and eosinophils at 24 h after the macroshock exposure to OA, compared with saline controls. A significant (P < 0.05) increase in the proportion of eosinophils also occurred in BAL fluid at 24 h after microshock OA challenge. Neutrophils, however, did not alter at 24 h, yet a late phase bronchoconstriction was recorded. Thus, macroshock (with mepyramine cover) and microshock (without mepyramine cover) OA challenges result in both early and late phase bronchoconstrictions. The late phase is associated with influx of eosinophils in both models but neutrophils only appear after the macroshock, indicating that late phase responses may not involve neutrophil infiltration to the airways.

Administration, Inhalation↗

PubMed1997

Lack of effect of nitric oxide inhibition on bronchial tone and methacholine-induced bronchoconstriction in man.

The role of nitric oxide (NO) as a bronchodilator has been studied in humans with controversial results. The aim of the present study was to investigate the role of endogenous NO on bronchial tone by studying whether nitric oxide synthase (NOS) inhibition with NGnitro-L-arginine-methyl-ester (L-NAME) influences basal bronchial tone, or potentiates methacholine-induced bronchoconstriction. In a preliminary experiment in five subjects, a significant reduction in exhaled NO was found after delivering L-NAME (15 mg in saline) (from 3.9 +/- 1.2 to 2.4 +/- 1.1 nmol min-1, P < 0.05). In nine healthy non-smokers, specific airway conductance (SGAW), as a measure of airway calibre, was recorded after delivering, in a double-blind, controlled vs. placebo fashion, both nebulized L-NAME and saline, at baseline and after methacholine-induced bronchoconstriction. There was no significant difference between the baseline SGAW values before and after delivering L-NAME (0.264 +/- 0.04 and 0.267 +/- 0.05 cm H2O-1 s-1, respectively). After pre-treatment with L-NAME, SGAW values during methacholine-induced bronchoconstriction were not different in comparison to values obtained after saline inhalation. It is concluded that decreased endogenous NO does not influence bronchial tone in healthy people, nor does it modify methacholine-induced bronchoconstriction.

Adult↗

PubMed2004

Asthma and exercise-induced bronchoconstriction in amateur endurance-trained athletes.

High-level endurance training contributes to the development of asthma and exercise-induced bronchoconstriction but the effect of moderate endurance training on airway function remains to be determined. The aim of this study was to evaluate the prevalence of physician-diagnosed asthma and/or exercise-induced bronchoconstriction in moderately endurance-trained athletes. Ninety-five Mediterranean amateur endurance-trained athletes filled out a questionnaire about respiratory disorders and underwent a resting spirometry. Mean training volume was 10 h per week. The prevalence of asthma was found to be 4.2 %. All the athletes with asthma plus another one (5.3 %) reported having exercise-induced bronchoconstriction. These percentages are in the same range as those from the general population and much lower than those observed in elite endurance athletes. In contrast to elite athletes, our amateur endurance-trained athletes seem not exposed to a higher risk of asthma or exercise-induced bronchoconstriction than the general population. We suggest that 10 h per week of moderate endurance training in a temperate climate area does not lead to respiratory disease.

Adolescent↗

PubMed2001

A comparison of the relaxant effects of olprinone and aminophylline on methacholine-induced bronchoconstriction in dogs.

UNLABELLED: IV aminophylline, a nonselective phosphodiesterase (PDE) inhibitor, is often used to treat an asthma attack during anesthesia. However, in some instances, aminophylline-resistant attacks are observed. Selective PDE3 inhibitors are now clinically available and have been reported to produce bronchodilation. Thus, we compared the relaxant effects of olprinone, a novel PDE3 inhibitor, and aminophylline on methacholine-induced bronchoconstriction. Dogs were anesthetized with pentobarbital. Bronchoconstriction was elicited with methacholine (0.5 microg/kg + 5.0 microg. kg(-1). min(-1)) and assessed as percentage of changes in the bronchial cross-sectional area (BCA; basal = 100%) monitored by bronchoscope. Initially, the relaxant effects of olprinone (n = 8; 0-1000 microg/kg) and aminophylline (n = 8; 0-50 mg/kg) were compared. The bronchial cross-sectional areas were assessed before and 30 min after methacholine infusion began and 5 min after each dose of olprinone or aminophylline. We then determined whether propranolol (0.4 mg/kg) reversed the relaxation induced by olprinone (1000 microg/kg) and aminophylline (50 mg/kg). Olprinone and aminophylline dose-dependently antagonized bronchoconstriction by 56.2% +/- 21.3% (SD) and 68.0% +/- 30.3% with -log 50% effective dose (mean) of 4.80 +/- 0.38 (15.8) microg/kg and 1.96 +/- 0.42 (10.9) mg/kg, respectively. Aminophylline 50 mg/kg significantly increased plasma epinephrine, whereas olprinone did not. In addition, propranolol significantly reduced aminophylline-induced relaxation, but not olprinone-induced relaxation. Therefore, the relaxant effects of olprinone are independent of plasma epinephrine, whereas aminophylline effects may partially result from increased circulating concentrations of epinephrine. IMPLICATIONS: We compared the relaxant effects of olprinone and aminophylline on methacholine-induced bronchoconstriction in dogs. The relaxant effects of olprinone are independent of plasma epinephrine, whereas the aminophylline effects may be partly caused by an increase in plasma epinephrine.

Aminophylline↗

PubMed1979

Effects of H1- and H2-receptor blocking agents on histamine-induced bronchoconstriction in non-asthmatic subjects.

1 Two studies have been carried out to investigate the effect of H1- and H2-receptor blocking agents on histamine-induced bronchoconstriction in non-asthmatic subjects. 2 The H2-receptor blocker cimetidine administered orally had no effect on histamine-induced bronchoconstriction on any of the subjects tested. In three of four subjects, the H1-receptor blocker, chlorpheniramine given orally, inhibited the effect of the histamine in the lung. 3 The effects of intravenous chlorpheniramine and cimetidine, both alone and in combination, upon histamine-induced bronchoconstriction, were also studied. Chlorpheniramine inhibited the effect of the histamine and this was significantly dose related. This was not so with cimetidine and there was no evidence that the dose response curve to chlorpheniramine was affected by the additional administration of cimetidine. 4 The results show that histamine-induced bronchoconstriction in non-asthmatic subjects is not mediated by H2-receptors, but it is likely that H1-receptors are involved.

Administration, Oral↗

PubMed1988

LTD4-induced bronchoconstriction in patients with asthma: lack of a vagal reflex.

The mechanism by which leukotriene D4 (LTD4) induces bronchoconstriction in man is unclear. We have investigated this mechanism by examining the effect of nedocromil sodium and ipratropium bromide on LTD4-induced bronchoconstriction in six mild asthmatic patients. The bronchoconstrictor response to increasing concentrations of inhaled LTD4 (0.08 to 100 nmol) was assessed by measuring changes in respiratory resistance (Rrs) at 6 Hz by the forced oscillation method. Results were expressed as the provocative dose causing 100% increase in Rrs (PD100). Neither nedocromil (4 mg) nor ipratropium (0.8 mg) showed significant effect on LTD4-induced bronchoconstriction in asthmatic subjects. These results suggest that in asthmatics LTD4-induced bronchoconstriction is unlikely to involve vagal reflexes.

Adult↗

PubMed1989

Bradykinin-induced bronchoconstriction: inhibition by nedocromil sodium and sodium cromoglycate.

1. The effects of inhaled nedocromil sodium and sodium cromoglycate on bradykinin-induced bronchoconstriction have been studied in a double-blind, placebo controlled study, in eight mild asthmatic subjects. 2. The subjects attended on four occasions. Fifteen minutes after drug pre-treatment a bradykinin challenge was performed. Increasing concentrations were inhaled until a greater than 40% fall in expiratory flow at 30% of vital capacity from a partial flow volume manoeuvre (V p30) was demonstrated. 3. Inhaled bradykinin (0.06-8.0 mg ml-1) caused dose-related bronchoconstriction with the geometric mean cumulative dose causing a 40% fall in V p30 (PD40) of 0.035 (95% CI: 0.02-0.07) mumol, after placebo inhalation, which was similar to that measured before the trial (0.04: 0.02-0.09 mumol). 4. Both nedocromil sodium (4 mg) and sodium cromoglycate (10 mg) gave significant protection (P less than 0.05) against bradykinin-induced bronchoconstriction (PD40 0.37: 0.19-0.72 mumol after nedocromil sodium and 0.22: 0.11-0.49 after sodium cromoglycate). 5. Since bradykinin-induced bronchoconstriction is probably neurally mediated we conclude that both nedocromil sodium and sodium cromoglycate have an action on neural pathways which may be useful in the control of asthma symptoms.

Adult↗

PubMed1989

Inhibition of bradykinin-induced bronchoconstriction in the guinea-pig by a synthetic B2 receptor antagonist.

1. Intravenous bradykinin (Bk) elicited bronchoconstriction in the anaesthetized ventilated guinea-pig which was not mimicked by the B1 receptor agonist, des-Arg9-Bk. 2. Bradykinin-induced bronchoconstriction was inhibited by the B2 receptor antagonist B4881, but not by the B1 receptor antagonist des-Arg9-Leu8-Bk. The effect of B4881 was short-lived. 3. The B2 receptor antagonist as B4881 was selective for bradykinin as B4881 did not significantly inhibit bronchoconstriction induced by i.v. bombesin, platelet activating factor, acetylcholine, histamine or vagal stimulation. 4. These results suggest that bradykinin-induced bronchoconstriction in the guinea-pig is via activation of a B2 receptor population and that B4881 is a selective B2 antagonist that may be useful for investigating the involvement of bradykinin in the lung.

Acetylcholine↗

PubMed1989

Role of histamine release in hypertonic saline induced bronchoconstriction.

In a study designed to determine the protective effect of the specific histamine H1 antagonist terfenadine on hypertonic saline induced bronchoconstriction, 10 asthmatic subjects underwent hypertonic saline challenge (3.6%) after premedication with placebo or terfenadine (120 mg) 12 and two hours before the challenge. Hypertonic saline was administered in a dose dependent manner and the response determined as the dose of hypertonic saline that induced a 20% fall in FEV1 (PD20 FEV1). FEV1 was on average 11% greater with terfenadine than with placebo given before the challenge with hypertonic saline. PD20 FEV1 was attenuated by a mean of 2.5 fold after terfenadine (geometric mean PD20 FEV1 was 22 litres after placebo and 56 l after terfenadine). There was substantial intersubject variation in the inhibitory effect of terfenadine on hypertonic saline induced bronchoconstriction: the ratio of the PD20 hypertonic saline after terfenadine to that after placebo ranged from 0.9 to 10.0. Terfenadine inhibited histamine induced bronchoconstriction in the eight subjects in whom it was tested, by 13 to 160 fold compared with placebo in four subjects and by greater than 2 to greater than 9 fold in the four who showed no response to the highest dose of histamine given (16 mg/ml). These results suggest that histamine release has a role in hypertonic saline induced bronchoconstriction in some individuals; other mediators or mechanisms may have a more prominent role in others.

Adult↗

PubMed1996

Exercise-induced bronchoconstriction by ethnicity and presence of asthma in British nine year olds.

BACKGROUND: The prevalence of exercise-induced bronchoconstriction among British children by ethnicity has not been studied. METHODS: Peak expiratory flow rate (PEFR) was measured before and after an exercise challenge test using a cycle ergometer in 593 nine year olds from Scottish and inner city English schools. Logistic regression analysis was carried out to assess the association between changes in PEFR with exercise by reported asthma, ethnicity, and sex. RESULTS: The probability of exercise-induced bronchoconstriction was greater among the asthmatics than in either the children without asthma attacks or wheeze, or in the children with only wheeze (p < 0.01). Asian children were 3.6 times more likely to have exercise-induced bronchoconstriction than white inner city children, and also were more likely to have exercise-induced bronchoconstriction than those from the other ethnic groups (p < 0.01). CONCLUSION: Exercise challenge can assess the prevalence of asthma in the community and detect under-reporting of asthma in ethnic minorities.

Black or African American↗

PubMed1985

Laryngeal constriction in normal humans during experimentally induced bronchoconstriction.

Changes in the size of the glottis with bronchoconstriction were assessed in six normal subjects following inhalation of histamine or methacholine. Measurements were made during both tidal breathing and panting at 2-3 Hz. The midexpiratory size of the glottis was decreased by a mean of 8% during bronchoconstriction compared with control during tidal breathing. Changes in midinspiratory size were inconsistent. During panting, the glottic size was unchanged from inspiration to expiration but decreased in 7 of 15 studies during bronchoconstriction. The decreases in expiratory size of the glottis during quiet breathing would lead to an elevated laryngeal resistance coupled with an increased lower airway resistance. Although this seems to be a paradoxical laryngeal response, it may contribute to maintaining hyperinflation during bronchoconstriction, thereby effectively enlarging the lower airways.

Adult↗

PubMed1986

Effects of induced bronchoconstriction on pulmonary blood flow.

Allergic bronchoconstriction may be associated with hemodynamic alterations due to changes in respiratory mechanics (or the associated changes in arterial blood gas composition) or the cardiovascular effects of chemical mediators. In an attempt to differentiate between these two possible mechanisms, we obtained measurements of hemodynamics, respiratory mechanics, and O2 consumption (VO2) in nine asymptomatic adult ragweed asthmatics before and after inhalation challenge with either ragweed extract or methacholine. We measured specific airway conductance (sGaw) by body plethysmography, pleural pressure with an esophageal balloon catheter, pulmonary blood flow (Q) and VO2 by a rebreathing technique, and heart rate. For a similar degree of bronchoconstriction after the two types of challenge (mean +/- SD sGaw 0.06 +/- 0.03 and 0.05 +/- 0.02 cmH2O-1 . s-1, P = NS), mean Q increased by 29 and 29%, and mean VO2 by 33 and 37% 15-20 min after ragweed and methacholine, respectively. Since heart rate did not change, there was a concomitant increase in mean stroke volume by 25 and 35%, respectively (P less than 0.05). The respiratory pleural pressure swings during quiet breathing and the rebreathing maneuver and the work of breathing during rebreathing also increased to a similar degree after the two types of challenge. These observations suggest that, if chemical mediators are released into the circulation during antigen-induced bronchoconstriction, their blood concentrations are too low for appreciable cardiovascular effects. The increase in rebreathing cardiac output during allergic and nonallergic bronchoconstriction is probably due to increases in intrathoracic pressure swings and in the work of breathing.

Adult↗