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PubMed2006

Clinical inquiries. What best prevents exercise-induced bronchoconstriction for a child with asthma?

Inhaled short-acting beta-agonists (SABAs) are most effective in preventing exercise-induced bronchoconstriction, followed by inhaled mast cell stabilizers and anticholinergic agents (strength of recommendation [SOR]: A, multiple randomized control trials [RCTs]). Less evidence supports the use of leukotriene antagonists and inhaled corticosteroids, either individually or in combination (SOR: B). Underlying asthma, which commonly contributes to exercise-induced bronchoconstriction, should be diagnosed and controlled first (SOR: C).

Adrenergic beta-Agonists↗
PubMed1990

Influence of antihistamine (astemizole) and anticholinergic drugs (ipratropium bromide) on bronchoconstriction induced by substance P.

Several studies have demonstrated that neuropeptides are present in bronchial tissue. The aim of this study was to evaluate in vivo the influence of antihistamine in comparison to an anticholinergic drug on bronchospasm induced by inhalation of substance P (SP). Seven moderate asthmatic patients (mean age = 34.4 +/- 8.9), five being female, were studied. The acetate salt of SP was prepared in 0.9% saline to produce a dose range of 23 to 184 x 10(-6) mol. Patients were studied on three separate days with an interval of 3 weeks between challenges. On the first day the dose of SP producing a 20% change in FEV1 was calculated from the individual semilogarithmic dose-response curve. On subsequent days, in a randomized double-blind manner, the patients were treated either with astemizole (20 mg BID for three days) and placebo ipratropium bromide or with placebo of astemizole (twice a day for three days) and with pressurized aerosol of ipratropium bromide (IB) (40 micrograms 20 minutes before the challenge). Two way analysis of variance was used for statistical analysis. Our results demonstrated that inhaled SP is able to produce a dose-response curve of bronchoconstriction with a geometric mean of PD20 of 50.51 x 10(-6) moles (37.38 to 68.19 x 10(-6) mol). Treatment with astemizole induced a geometric mean PD20 of 65.51 x 10(-6) mol (33.02 to 130.21 x 10(-6) mol) and the premedication with the IB induced a significant (P less than .05) shift of dose-response curve to SP (geometric mean PD20 = 109.1 x 10(-6) mol; 58.67 to 204.05 x 10(-6) mol). Our results demonstrated that bronchoconstriction induced by SP could be attributed to a weak cholinergic activation and not to histamine release.

Administration, Inhalation↗
PubMedDate not supplied

Methoxyphenamine inhibits histamine-induced bronchoconstriction in anaesthetized guinea-pigs and histamine-induced contractions of guinea-pig ileum in vitro.

Measurements were made of the effects of methoxyphenamine hydrochloride on histamine-, acetylcholine- and U46619-induced bronchoconstriction in pentobarbitone-anaesthetized guinea-pigs, and on histamine- and acetylcholine-induced contractions of guinea-pig ileum in vitro. Methoxyphenamine (20 mg/kg, i.v.) did not affect bronchoconstriction induced by acetylcholine or the thromboxane A2-mimetic U46619. However, it produced a parallel rightward shift [2.94-(1.79, 4.41) fold, 95% confidence limits in parentheses] of the curve relating bronchoconstrictor responses to log-dose of histamine at a total dose of 13 mg/kg, i.v., which was not significantly different from the shift [3.30-(1.93, 5.56) fold] produced by 3 micrograms/kg, i.v., of the histamine antagonist mepyramine maleate. Histamine-induced contractions of the isolated guinea-pig ileum were antagonized by methoxyphenamine (10(-5) to 10(-3) M). The histamine log-concentration-response curve was shifted to the right in a parallel manner by methoxyphenamine (10(-5) to 10(-4) M), without depression of maximum responses. However, at higher concentrations, maximum responses were reduced. The slope of the Schild plot was significantly different from -1. The degree of the rightward shift of the concentration-response curves to histamine, produced by 10(-5) M of methoxyphenamine [3.90-(2.83, 4.97) fold], was not significantly different from that produced by 3 x 10(-9) M of mepyramine [4.60-(2.86, 6.52) fold]. Methoxyphenamine, at concentrations of 10(-5) to 3 x 10(-4) M, had no significant effect on responses of guinea-pig ilea to acetylcholine (10(-9) to 10(-5) M). These results indicate that methoxyphenamine antagonizes the effects of histamine both in vivo and in vitro. In vitro studies indicate a noncompetitive antagonism.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1990

Inhibition of adenosine 5'-monophosphate- and methacholine-induced bronchoconstriction in asthma by inhaled frusemide.

Recent studies have shown that inhaled frusemide exerts a protective effect against various bronchoconstrictor stimuli in asthma including exercise, fog and allergen. Since mast cell activation seems to be a component of bronchoconstriction by these stimuli it is possible that inhibition of mediator release accounts for some or all of the inhibitory effects of frusemide in asthma. Since inhaled adenosine 5'-monophosphate (AMP) is another stimulus that produces bronchoconstriction by augmenting mast cell mediator release, we have investigated the ability of this drug to antagonise the airway effects of inhaled AMP and methacholine in a randomized, placebo-controlled, double-blind study of 12 asthmatic subjects. Inhaled frusemide (approximately 28 mg) administered 5 min prior to challenge increased the provocation concentration of inhaled AMP and methacholine required to reduce forced expiratory volume in one second (FEV) by 20% from baseline from 30 to 96 mg.ml-1 (p less than 0.01) and from 1.1 to 1.8 mg.ml-1 (p less than 0.01), respectively. The protection that frusemide afforded against AMP was significantly greater than that against methacholine (p less than 0.05). These data suggest that inhaled frusemide may serve as a functional antagonist against a smooth muscle spasmogen, such as methacholine, possibly by augmenting prostanoid generation. Its more potent activity against AMP and other bronchoconstrictor stimuli, that are considered to involve mast cell mediators, suggests an additional action on mast cell functions possibly at the level of the Ca++/Mg(++)-ATPase.

Adenosine Monophosphate↗
PubMed1990

Bradykinin-induced bronchoconstriction in guinea pig in vivo: role of neural mechanisms.

The mechanism of bradykinin-induced bronchoconstriction was studied in anesthetized guinea pigs after both i.v. administration and direct airway instillation. We monitored airway opening pressure as an index of airway caliber, and the provocative dose of bradykinin required to produce 100% increase in airway opening pressure (PD100) was determined. Animals were pretreated with propranolol (1 mg/kg i.v.) to inhibit adrenergic bronchodilatation. After i.v. administration, the bronchoconstrictor dose-response curve to bradykinin (PD100 = 0.93 nmol/kg) was shifted significantly to the right by atropine (PD100 = 2.34 nmol/kg, P less than .05) and indomethacin (PD100 = 61.7 nmol/kg, P less than .05). Depletion of tachykinins by capsaicin pretreatment had no significant effect on the response to i.v. bradykinin. After tracheal instillation, the bronchoconstrictor dose-response curve to bradykinin (PD100 = 24.5 nmol) was shifted to the right by atropine (PD100 greater than 150 nmol, P less than .05) and capsaicin pretreatment (PD100 greater than 150 nmol, P less than .05). After atropine the response to instilled bradykinin was almost abolished in capsaicin-pretreated animals. Indomethacin had no effect on the bronchoconstrictor response to instilled bradykinin. We conclude that i.v. bradykinin causes bronchoconstriction predominantly by the release of cyclooxygenase products but that a cholinergic reflex is also involved, whereas sensory neuropeptides are not important. By contrast the bronchoconstrictor response to instilled bradykinin is mediated by neural mechanisms involving both cholinergic nerves and sensory neuropeptides but not by cyclooxygenase products.

Animals↗
PubMed1989

Effect of nedocromil sodium and sodium cromoglycate against bronchoconstriction induced by inhaled adenosine 5'-monophosphate.

In this randomized, double-blind, placebo controlled study, the effect of prior inhalation of nebulized sodium cromoglycate (SCG) (7.3 +/- 0.6 mg) and nedocromil sodium (NED) (7.5 +/- 0.6 mg) was observed on adenosine 5'-monophosphate (AMP)-induced bronchoconstriction in 11 non-atopic asthmatic subjects. The geometric mean provocation doses of methacholine and AMP required to produce a 20% decrease in forced expiratory volume in one second (FEV1) (PD20FEV1) were 0.6 (0.1-18.8) and 5.1 (0.8-130.7) mumole respectively. The repeatability of the AMP challenge procedure for PD20FEV1 was within one doubling dose difference. SCG and NED, administered 30 min prior to bronchoprovocation with AMP, displaced the AMP dose-response curve to the right by 9.6 (1.5-41.6) (p less than 0.01) and 22.2 (3.7-89.1) (p less than 0.01)-fold, respectively, the difference between the two drugs being significant (p less than 0.05). There was a significant correlation (r = 0.7, p = 0.02) between the log dose ratios for PD20FEV1 for SCG and NED. We conclude that both SCG and NED protect against AMP-induced bronchoconstriction, NED being at least 2.3 (0.7-11.5)-fold more potent than SCG, and that they achieve this effect by a similar mechanism(s).

Adenosine Monophosphate↗
PubMed1989

[Inhibitory effect of procaterol (beta 2 agonist) on the release of cyclooxygenase products during antigen-induced bronchoconstriction in the guinea pig in vivo].

The purpose of this study was to investigate whether procaterol (beta 2 agonist) inhibits the release of cyclooxygenase products in bronchoalveolar lavage fluid (BALF) during in vivo allergic bronchoconstriction in passively sensitized guinea pigs. Antigen-induced bronchoconstriction was significantly inhibited by pretreatment with procaterol. The concentrations of 6-keto-PGF1 alpha, PGF2 alpha and TXB2 in BALF significantly decreased in guinea pigs pretreated with inhaled procaterol. The concentration of TXB2, which is the stable metabolite of TXA2, a strong bronchoconstrictor, was especially markedly decreased compared with that in the control animals. These data indicate that procaterol (beta 2 agonist) may inhibit the release of chemical mediators during allergic reactions as well as directly decrease the contractility of airway smooth muscle. Consequently, regular inhalation of procaterol may be clinically useful for prophylaxis of bronchial asthma.

Administration, Inhalation↗
PubMed1989

Effect of nisoldipine (BAY k 5552) on methacholine-induced bronchoconstriction in patients with nonspecific bronchial hyperreactivity.

The purpose of this study was to determine whether a new calcium antagonist, nisoldipine (BAY k5552), exerted protection against methacholine-induced bronchoconstriction in subjects with hyperreactive airways. Twelve symptomless rhinitic and/or asthmatic patients with previously demonstrated bronchial hyperreactivity to methacholine were treated with placebo or nisoldipine (10 mg) according to a randomized, double-blind, crossover, placebo-controlled study design. Airway reactivity was examined through changes in response to methacholine challenge three hours after drug or placebo administration. Nisoldipine, in comparison to placebo, produced a weak but significant rise of provocative dose of methacholine responsible for a 15% fall in FEV1 (P less than .01). The data suggest that a single dose of 10 mg of nisoldipine is able partially to counteract methacholine-induced bronchoconstriction in atopic subjects with nonspecific airway hyperresponsiveness.

Asthma↗
PubMed1989

[Airway responsiveness measured by body plethysmograph connecting a circuit of an inhalation system of serially concentrated bronchoconstrictant].

We developed a new methodology to examine the bronchial response to the bronchoconstrictants, acetylcholine and methacholine. An inhalation device was connected to the body plethysmograph circuit so that a minute inhalation of serially concentrated bronchoconstrictant could be quickly switched to the circuit of the measurement of the airway resistance. The following were calculated: airway responsiveness in terms of sensitivity, provocative dose to increase the airway resistance up to 35% from the baseline. PC35 or PD35 and the reactivity, the slope of the declining specific airway conductance and %delta SGaw. The airway responsiveness was examined in asthmatics, COPD outgrew -childhood asthma patients and normal subjects. These three groups were categorised differently from each other in both sensitivity and reactivity.

Acetylcholine↗
PubMed1988

Effect of terfenadine on the bronchoconstriction induced by ultrasonically nebulized distilled water.

Ultrasonically nebulized distilled water (UNDW) has been shown to induce bronchoconstriction in asthmatics. The proposed mechanism is through changes in osmolarity of the airway fluids and subsequent release of mediators from airway mast cells. We investigated whether terfenadine has a protective effect on UNDW challenges. Twelve mild-to-moderate asthmatics responded to screening a methacholine and UNDW challenge. For four hours after the ingestion of 0, 120, and 240 mg of terfenadine pulmonary responses were performed, followed by a UNDW challenge. Nine of 12 subjects dropped 20% after 120 mg and after 240 mg. There was a suggestion of a protective effect at 120 mg (P = .054), which was significant at 240 mg (P = .012) when the areas under the dose-response curves were compared. Bronchoconstriction induced by UNDW may in part be caused by histamine release and was attenuated by an oral antihistamine.

Adolescent↗
PubMed1986

Lack of protective effect of high-dose ipratropium on bronchoconstriction following exercise with cold air breathing in patients with mild asthma.

To evaluate the preventive effect of inhaled ipratropium powder on low-grade bronchoconstriction elicited by breathing cold air during exercise, we subjected 10 adult patients with mild asthma to four identical treadmill exercise tests. The temperature of inhaled air during exercise was -9 +/- 1 degree C. Sixty minutes before exercise, the patients inhaled either placebo or 0.2, 1, or 2 mg of ipratropium powder according to a cross-over, double-blind arrangement. The mean post-exercise fall from the post-treatment pre-exercise values in the four treatment groups was 14, 14, 16 and 16% for FEV1, and 59, 52, 52 and 55% for SGaw, respectively. We concluded that doses of ipratropium up to 20-50 times higher than those known to have a marked effect on resting bronchomotor tone in clinically stable asthma did not blunt the bronchoconstriction response following exercise with cold air breathing in our patients with mild asthma.

Adolescent↗
PubMedDate not supplied

[The effects of different inhibitors on bronchoconstriction induced by leukotriene D4 in isolated and perfused guinea pig lung].

The effects of selective inhibitions of both cyclo-oxygenase and lipoxygenase pathways were studied in the isolated, perfused and ventilated guinea-pig lungs. Leukotriene D4 (0.3 nmol) induced a significant bronchoconstriction. This effect was significantly inhibited by IPL 55712 (a SRS-A antagonist) and by Imidazole or Dazoxiben (specific thromboxane synthetase inhibitors), but aspirin and indomethacin were without significant effect on this broncho-constriction. Our results suggest that the principal component of leukotriene D4 induced bronchoconstriction in guinea-pig lungs is primary.

Animals↗
PubMedDate not supplied

[Circadian variations of bronchoconstriction in asthmatic children].

In order to determine the magnitude of circadian variations in bronchoconstriction, we examined modifications of the spirometry observed during the 24-hr in a group of asthmatic (31 males, mean age = 8 years, 6 months). Particular attention was paid to the forced expiratory volume in 1 sec. (FEV1) and the forced vital capacity (FVC). We were thus able to compare in single patients 43 spirometry pairs between morning (between 8 and 10 am) and early afternoon (between 1 and 4 pm), 46 pairs between morning and evening (between 6 and 10 pm) and 54 between 2 consecutive mornings. The results of this study, substantially similar for the FEV1 and the FVC, show that the mean values obtained at different hours during the day and in two consecutive mornings were almost superimposable. On the other hand, the mean values and the standard deviations of the differences between two determinations in single patients are high. The percentage of patients who present significant modifications (greater than 10%) of FEV1 or of FVC at different hours of the day is also quite high. Moreover these variations seem directly related to the baseline spirometric value. Although the literature frequently outlines the existence of a circadian rhythm in the modifications or airways patency (maximum bronchoconstriction in the morning and minimum in the evening), in the asthmatic, however, the fast variations in the bronchial tone can be such as to mask this cyclic rhythm.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1988

Changes in neural drive (EMGd) and neuromuscular coupling during histamine-induced bronchoconstriction in patients with asthma.

This study was undertaken in order to assess the neural drive to the respiratory muscles and the inspiratory neuromuscular coupling in patients with bronchial asthma during histamine-induced bronchoconstriction. Bronchoconstriction was produced in a graded fashion, with histamine phosphate aerosol of increasing dose, in twelve asymptomatic asthmatic patients and was measured by FEV1. Inspiratory drive was measured by electromyographic activity of the diaphragm (EMGd) and the coupling of the neural drive to the respiratory muscles was assessed by the relationship of mouth occlusion pressure (P0.1) to EMGd. During the test we also measured electromyographic activity of the inspiratory intercostal (EMGint), sternomastoid (EMGsm) and expiratory abdominal (EMGab) muscles. Histamine caused a significant decrease in FEV1, a significant increase in P0.1, EMGd, EMGint, and a relevant increase in EMGsm, with no substantial increase in EMGab. An inverse significant relationship between the change in FEV1 and changes in P0.1, EMGd and EMGint and a significant correlation between the change in FEV1 and in the P0.1/EMGd ratio were observed. We conclude that a progressive increase in bronchospasm is accompanied by a progressive increase in respiratory neural drive and decrease in neuromuscular coupling. This could be caused both by an increase in lung volume and a lack of abdominal expiratory muscle recruitment.

Adult↗
PubMed1988

Bronchoconstriction due to exercise combined with cold air inhalation does not generally influence bronchial responsiveness to inhaled histamine in asthmatic subjects.

We investigated immediate and late changes in airway responsiveness to histamine, after bronchoconstriction due to exercise combined with inhalation of cold air, in ten asthmatic subjects who came on six days. On the first visit, the provocation concentration producing 20% fall in FEV1 (PC20) histamine was obtained. After functional recovery, each subject walked on a treadmill whilst breathing dry, cold air. This resulted in an immediate fall greater than 15% (mean +/- SD = 31.9 +/- 11.0%) in forced expiratory volume in one second (FEV1). Following recovery, PC20 was measured again. FEV1 was then monitored for up to 6-8 h. PC20 was measured then and on the two following days at the same time of the day. Subjects were studied on three control days using the same design except that a resting period replaced the exercise with cold air. The mean changes in PC20 at each interval after exercise combined with cold air were not statistically significant. Physiologically significant changes were obtained in only two subjects, reaching a maximum 8 h after the manoeuvre. In these subjects, changes in PC20 were reproducible during a second series of visits. It is concluded that bronchial responsiveness to histamine is not generally influenced by the bronchoconstriction due to exercise combined with cold air.

Adolescent↗
PubMed1985

The significance of the reflex bronchoconstriction provoked by gastroesophageal reflux in bronchial asthma.

To demonstrate the existence and assess the magnitude of reflex bronchoconstriction in asthmatics, triggered by gastroesophageal reflux, pulmonary function studies (forced expiratory spirogram, flow-volume loops and airway resistance) were performed during a Bernstein test in 21 adult patients with intrinsic asthma and in 15 controls. Six asthmatics and 7 controls had symptomatic reflux test and a positive standard acid reflux test. Bernstein test was positive in all symptomatic individuals and in 2 asthmatics with a negative standard acid reflux test. Changes in pulmonary function occur only in asthmatics with symptomatic reflux. Decreases were: FEV1 8.4 +/- 3.4; FEF25-75% 45 +/- 7.3; Vmax 15 +/- 8.4; and Sgaw 16 +/- 3.7. Although changes were statistically significant (p less than 0.05), the magnitude of decrease is rather small and unlikely to be felt by an asthmatic or produce wheezy dyspnea. Therefore, even though the presence of acid in the lower esophagus may produce reflex bronchoconstriction in some asthmatics with symptomatic reflux, this appears to be of little significance.

Adult↗
PubMedDate not supplied

[Effects of verapamil and propranolol on bronchoconstriction induced by leukotriene D4 in the isolated perfused guinea pig lung].

The effects of verapamil and propranolol on the LTD4-induced bronchoconstriction were studied in the isolated, perfused and ventilated guinea pig lungs. Verapamil (4.10(-5) et 1, 2.10(-4)M.1(-1], a calcium antagonist, produces a significative inhibition of LTD4-induced bronchoconstriction. On the other hand, propranolol (10(-7)M and 10(-4)M) does not increase the constrictor effects of LTD4 in guinea-pig isolated lung. These first results obtained in guinea-pig lung, confirmed the protective effect of verapamil, effect previously demonstrated in vivo or in vitro by using lung parenchymal strips. We have also confirmed the difference between the in vivo and in vitro effects of propranolol.

Animals↗