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PubMed1994

Effect of theophylline on airway responsiveness to methacholine and on exercise-induced bronchoconstriction.

The aim of this study was to compare the relative effect of (1) a single dose of a rapid release theophylline, (2) treatment for 1 week with a sustained release theophylline, and (3) placebo after a washout period of at least 2 weeks on bronchial hyperresponsiveness to methacholine and on exercise-induced bronchoconstriction in 14 mildly asthmatic children. A dose of rapid release theophylline increased geometric mean (GM) PC20 (mg/mL) for methacholine from 0.25 to 0.85 (P < .001) at a mean (+/- SD) serum theophylline concentration of 9.5 +/- 2.5 mg/L (52.3 +/- 14.24 mumol/L). After 1 week on a slow release theophylline, GM PC20 increased to 0.41 (P < .01) at a mean serum theophylline concentration of 13.63 +/- 4.7 mg/L (74.9 +/- 25.8 mumol/L), (P < .01) compared with rapid release theophylline. The difference in PC20 between both theophylline treatments was statistically significant (P < .05). No significant changes in PC20 were noted after placebo compared with baseline values. During baseline and after placebo mean maximum FEV1 fall (MMFF) after exercise was 40 +/- 19.9% and 31.7 +/- 15.5%, respectively (n.s.). After a dose of rapid release theophylline, MMFF on exercise test was 8.7 +/- 8.2% (mean serum theophylline concentration 10 +/- 3.2 mg/L (55.4 +/- 17.82 mumol/L)), P < .001 compared with baseline and placebo. After 1 week of treatment with slow release theophylline, MMFF was 26.2% +/- 18.3 (mean serum theophylline concentration 12.2 +/- 3.9 mg/L (67.43 +/- 21.5 mumol/L)) (P = .01 and P = .30 compared with baseline and placebo, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1994

[The role of parasympathetic nerve on hyperventilation-induced bronchoconstriction in sensitized rabbits].

We have demonstrated that hyperventilation-induced bronchoconstriction (HIB) is observed in sensitized rabbits, and that histamine may play a role in HIB. To investigate the role of parasympathetic neurotransmission in HIB, the effects of atropine and vagotomy on HIB were examined. Japanese white rabbits were sensitized with ovalbumin. They were then anesthetized and paralyzed with pancuronium, and then mechanically ventilated (TV: 7 ml/kg, RR: 40/min). The rabbits were divided into the following three groups: I) control group (n = 7), II) atropine-treated group (n = 6), III) bilateral vagotomy group (n = 6). Hyperventilation was performed at TV: 7 ml/kg, RR: 120/min for 15 min in dry room air containing 5% CO2. Total lung resistance (RL) and dynamic compliance (Cdyn) were measured before and at 0, 5, 15 and 30 minutes after hyperventilation. RL increases significantly at 5 minutes in group 1, but this change was significantly less marked in groups 2 and 3. However Cdyn was not significant change in each group. We conclude that parasympathetic neurotransmission may play an important role in HIB of sensitized rabbits.

Animals↗
PubMed1994

Adenosine-induced bronchoconstriction and contraction of airway smooth muscle from allergic rabbits with late-phase airway obstruction: evidence for an inducible adenosine A1 receptor.

Recently, there has been an increasing interest in adenosine as a potential mediator of allergic asthma. In the present study, we used the allergic rabbit model developed in our laboratory to study the airway responses to adenosine and receptor binding in allergic lung vs. normal. Neonatal, pathogen-free rabbit litter mates were injected intraperitoneally within 24 hr of birth with ragweed pollen extract (1 mg/ml) to produce preferentially allergen-specific immunoglobulin E. Immunization produced bronchial airway hyperresponsiveness. Aerosolized adenosine (0.156-10 mg/ml) caused a dose-dependent bronchoconstriction (PC50 adenosine = 1.64 +/- 0.84 mg/ml). 9-Chloro-2-(2-furyl)[1,2,4]triazole[1,5- c]quinazolin-5-amine (CGS-15943), a nonxanthine adenosine receptor antagonist, significantly inhibited the adenosine-induced airway obstruction in term of dynamic compliance (P < .05). Adenosine also increased the lung resistance in a dose-dependent manner which was significantly inhibited by CGS-15943 (P < .05). Nonimmunized, pathogen-free, age-matched rabbits (control) did not respond to adenosine at these same concentrations. Adenosine also produced a concentration-dependent (10(-9)-10(-4) M) contraction of isolated tracheal and bronchial airway rings in vitro from allergic rabbits but had no detectable effect on normal rabbit airway smooth muscle. Peripheral airway smooth muscles (secondary and tertiary) were more responsive to adenosine than central (tracheal) airways. The contraction produced by 10(-4) M adenosine in primary, secondary and tertiary airways was 90, 135 and 265% of the contraction produced by 50 mM KCl, respectively. CGS-15943 (10(-7) M) significantly inhibited the adenosine-induced contraction (P < .05) shifting the dose-response curve to the right.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1993

Factors contributing to dyspnoea during bronchoconstriction and exercise in asthmatic subjects.

The purpose of the present study was to identify: 1) whether dyspnoea during bronchoconstriction and exercise is related, in asthmatic subjects; and 2) to what extent baseline pulmonary function and respiratory muscle strength contribute to dyspnoea under both conditions. One hundred and seventy five consecutive subjects, referred with suspected asthma, rated the intensity of dyspnoea (Borg scale 0-10): 1) during the administration of doubling concentrations of methacholine to 32 mg.ml-1 methacholine, or until the baseline forced expiratory volume in one second (FEV1) was reduced by 20%; and 2) during incremental cycle ergometry (100 kpm.min-1 each minute) to maximal capacity. 138/175 subjects achieved a 20% reduction in their baseline FEV1; 18 of the 138 were excluded, 2 children and 16 with complicating pulmonary disorders (diffusing capacity of the lung for carbon monoxide (DLCO) and/or total lung capacity (TLC) < 70% predicted). The remaining 120 out of 175 constituted the study population. Dyspnoea following a 20% reduction in the baseline FEV1 (Dys20%) was linearly interpolated, using the rating of dyspnoea and the FEV1 at the two final concentrations of methacholine. In the 120 asthmatic subjects, the mean intensity of dyspnoea was "moderate" (2.9, SD 1.91; Borg 0-10) and the intensity across subjects was not significantly related to baseline FEV1, vital capacity (VC), FEV1/VC, DLCO, TLC and maximal static inspiratory pressure (MIP), alone or in combination.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1993

Effect of inhaled disodium cromoglycate and nedocromil sodium on propranolol-induced bronchoconstriction.

We conducted a randomized, double-blind, placebo-controlled study on the effect of disodium cromoglycate (DSCG) and nedocromil sodium (NED) on propranolol-induced bronchoconstriction (PIB) in 12 asthmatic subjects 10 to 53 years of age. Placebo (saline solution) and active drugs (10 mg) were aerosolized 30 minutes before bronchoprovocation with inhaled propranolol. Bronchial response to propranolol was expressed as the cumulative dose provoking a 20% fall in FEV1 (PD20P) and given in mumol. Reproducibility of PD20P was estimated before and after the days of study. PD20P varied within two doubling doses. Disodium cromoglycate and NED had no significant effect on baseline lung function. Although, geometric mean PD20P values (+/- GSEM) recorded after DSCG (7.24 mumol +/- 1.31) and after NED (9.22 mumol +/- 1.26) were higher than values recorded after placebo (6.55 mumol +/- 1.31), these differences were not statistically significant. A greater than 2-fold increase in PD20P was noted after NED in three subjects and in one subject after DSCG. We conclude that both DSCG and NED only modestly alter PIB, with some between subject differences.

Administration, Inhalation↗
PubMed1993

Occupancy of platelet receptors for platelet-activating factor in asthmatic patients during an allergen-induced bronchoconstrictive reaction.

The administration of platelet-activating factor (PAF) to human subjects triggers asthma-like responses. We investigated whether a bronchoconstrictive reaction was accompanied by the release of PAF in the circulation of allergic asthmatics. The appearance of PAF was assessed by measuring the number of freely accessible PAF-receptors on platelets in vitro, assuming that the contact between platelets and PAF in vivo would reduce the receptor binding of [3H]PAF in vitro. 16 asthmatics were challenged twice, first with buffer and the next day with allergen. A comparison between receptor binding after provocation with the data of the same patients after allergen challenge revealed a significant difference in PAF binding (P = 0.034), with an average decrease of 14% immediately after allergen challenge followed by a return to control values after about 4 h and a transient increase of 9% at 7 h after provocation. The decrease in accessible PAF receptors was accompanied by a slight decrease in platelet count in peripheral blood between 30 min and 4 h after allergen challenge. The platelet counts recovered to the original values afterwards. These data support the concept that in patients with allergic asthma PAF is secreted in the circulation. The contact between PAF and the platelets may trigger the transient sequestration of platelets, possibly in the lung. Thus, PAF and platelets may contribute to the pathogenesis of allergic asthma.

Adolescent↗
PubMed1995

[Inhibitory effect of low molecular weight heparin on the bronchoconstriction in ovalbumin-sensitized guinea pigs after antigen exposure].

To elucidate the effect of low molecular weight heparin (LMWH) on the bronchoconstriction, we examined the serial changes of the resistance of respiratory system (Rrs) in ovalbumin (OA)-sensitized guinea pigs after antigen exposure. After sensitization of guinea pigs with repeated OA inhalation, Rrs was measured at immediate asthmatic response (IAR) and late asthmatic response (LAR) with or without LMWH inhalation. Alteration in the number of inflammatory cells of the lung by LMWH inhalation was examined in the broncholaveolar lavage fluid (BALF) and in the histological sections of airway walls. Peak Rrs at 1 min up to 9 min, except 8 min, after antigen exposure significantly decreased by the pretreatment with LMWH inhalation as compared with saline inhalation. Peak Rrs at LAR (after 4 hours up to 24 hours, except 6 hours) also showed a significant decrease in the pretreatment with LMWH inhalation. Pretreatment of LMWH exhibited a decrease of eosinophil percentage in BALF (5.5 +/- 1.2% from 8.2 +/- 0.4% in saline inhalation) and a decrease of infiltrated eosinophil count in airway walls (71.0 +/- 7.3 from 155 +/- 15.8 in saline inhalation). These data show LMWH might play an important role as an inhibitory factor to bronchial asthma.

Administration, Inhalation↗
PubMed1996

Alpha-adrenergic bronchoconstriction in man.

In normal as well as in asymptomatic subjects, inhaled norepinephrine (NE) induced bronchoconstriction and respiratory asynchronism only after pretreatment by propranolol. However, lower doses of beta-receptor blocker were needed in asthmatics to reveal NE constrictive properties. These airways resistance increases were prevented by phentolamine. These pharmacological data indicate that the resting bronchial tone is relaxed permanently by beta-adrenergic receptors stimulation whose suppression unmasks alpha-induced constriction. Bronchial relaxing properties predominate normally in man and in guinea pigs, as previously demonstrated (Marcelle, 1996).

Administration, Inhalation↗
PubMed1997

Atrial natriuretic peptide prevents bronchoconstriction in vitro.

Under in vitro conditions atrial natriuretic peptide (ANP) caused specific relation of bronchoconstriction induced by tosyl arginine methyl ester (TAME) on rat trachea. This supports the hypothesis that ANP is a relaxant of airway as well as vascular smooth muscle and since lung tissue contains ANP and ANP receptors, it is hypothesized that the lungs may be a target organ for ANP. It is concluded that ANP had definite bronchodilating properties on rat trachea mounted in vitro and could be a possible antagonist of TAME.

Animals↗
PubMed1997

Attenuation by phosphodiesterase inhibitors of lipopolysaccharide-induced thromboxane release and bronchoconstriction in rat lungs.

Exposure of perfused rat lungs to lipopolysaccharides (LPS) causes induction of cyclooxygenase-2 followed by thromboxane (TX)-mediated bronchoconstriction (BC). Recently, phosphodiesterase (PDE) inhibitors have received much interest because they not only are bronchodilators but also can suppress release of proinflammatory mediators. In the present study, we investigated the effect of three different PDE inhibitors on TX release and BC in LPS-exposed perfused rat lungs. The PDE inhibitors used were motapizone (PDE III specific), rolipram (PDE IV specific), and zardaverine (mixed PDE III and IV specific). At 5 microM, a concentration at which all three compounds selectively block their respective PDE isoenzyme, rolipram (IC50 = 0.04 microM) and zardaverine (IC50 = 1.8 microM) largely attenuated the LPS-induced BC, whereas motapizone was almost ineffective (IC50 = 40 microM). In contrast to LPS, BC induced by the TX-mimetic U46619 was prevented with comparable strength by motapizone and rolipram. In LPS-treated lungs, the TX release was reduced to 50% of controls by rolipram and zardaverine but was unaltered in the presence of 5 microM motapizone. Increasing intracellular cAMP through perfusion of db-cAMP or forskolin (activates adenylate cyclase) also reduced TX release and BC. We conclude that PDE inhibitors act via elevation of intracellular cAMP. Although both PDE III and PDE IV inhibitors can relax airway smooth muscle, in the model of LPS-induced BC, PDE IV inhibitors are more effective because (in contrast to PDE III inhibitors) they also attenuate TX release.

Animals↗
PubMed1988

Duration of effect of gallopamil, a calcium channel blocker, on methacholine-induced bronchoconstriction.

We previously demonstrated a modest but significant protective effect of inhaled gallopamil (D600), the methoxy derivative of verapamil, against methacholine-induced bronchoconstriction; however, the duration of the protective effect of this and other calcium channel blockers is unknown. We therefore evaluated the duration of this protective effect in 15 asthmatic subjects in a prospective, placebo-controlled trial. Methacholine challenges (Cockcroft method) were performed 2 hours before and 30 minutes after the administration of placebo, and 1 mg and 10 mg of inhaled gallopamil. Gallopamil did not alter resting airway caliber, but significantly increased the concentration of methacholine required to decrease the FEV1 20% 30 minutes after the dose. Results with both the 10-mg and 1-mg doses were significantly different from placebo, but not from each other. The duration of this protective effect was transient in the group as a whole; the mean drug activity ratios were not significantly different with this sample 2.5 hours after the dose. Thus the short duration of effect limits the potential clinical usefulness of gallopamil in suppressing the signs and symptoms of chronic asthma.

Adolescent↗
PubMedDate not supplied

Refractoriness to bronchoconstriction following hyperventilation with cold dry air.

Fifteen subjects undertook repeated periods of hyperventilation of cold dry air and hyperventilation of warm humidified air followed by cold dry air. Hyperventilation of cold dry air induced a biphasic response with initial bronchodilatation followed by bronchoconstriction. However, exercise produced a greater rise in forced expiratory volume in 1 second (FEV1) than hyperventilation alone. Hyperventilation of cold dry air resulted in a period of refractoriness to a second stress of the same type. Refractoriness induced by exercise or hyperventilation of cold dry air may be the result of refractoriness of the trigger site in the large airways.

Adolescent↗
PubMed1996

Speeds of action of single doses of formoterol and salbutamol compared with placebo in reversing methacholine-induced bronchoconstriction.

We compared the speeds of action of two doses of the long acting beta-agonist formoterol (12 micrograms and 24 micrograms) with those of salbutamol (400 micrograms) and placebo using a double-blind, randomized, cross-over study design in 16 asthmatic subjects. A methacholine test was used on four separate study days to produce a standardized degree of bronchoconstriction (a decrement in FEV1 > or = 20%) and one of the study medications as dry powder was administered immediately afterwards via an Aerolizer inhaler device. The speeds of recovery were estimated from measurements of FEV1 over the following 2-90 min. All active treatments produced significantly greater bronchodilation than placebo as early as 2 min after administration, and their peak effects within 10 min; and no significant differences were noted between them. Mean recovery times by 50% of the FEV1 decrement provoked by methacholine were significantly shorter for the active medications: 5.7 min (formoterol 24 micrograms), 6.4 min (salbutamol 400 micrograms), 10.2 min (formoterol 12 micrograms), and 53.1 min (placebo); the respective times for recovery by 80% being 18.0, 17.4, 22.1, and 83.3 min. We conclude that single doses of the dry powder formulations of all three active treatments produce rapid and effective bronchodilation. This conclusion should not, however, be extrapolated to the regular use of these medications, since differential down-regulation and tachyphylaxis may then exert an influence.

Adolescent↗
PubMed1981

Standardization of work intensity for evaluation of exercise-induced bronchoconstriction.

Reactivity of airways to 6 min of graded intensity treadmill work was studied in nine asthmatic and 15 non-asthmatic subjects. After performing a progressive VO2 max treadmill test, each subject completed five 6-min exercise tests at selected intensities: 40, 60, 80, and 100% VO2 max; and at 80% of VO2 max predicted from heartrate. Pulmonary function measures recorded after exercise demonstrated a direct relationship between work intensity and exercise induced bronchoconstriction (EIB) for both groups, with the asthmatics showing their lowest values at 80% VO2 max. Heartrate-set work intensities produced a wide range of aerobic demand, thus significantly increasing the variability of the EIB response recorded.

Adult↗
PubMed1977

Plasma catecholamines in exercise induced bronchoconstriction.

Plasma nor-epinephrine (NE) and epinephrine (E) levels at rest and immediately after exercise were estimated in 8 patients with asymptomatic extrinsic allergic bronchial asthma. The patients had a normal airway resistance at rest and developed a marked bronchoconstriction (EIB) during exercise, which could be prevented by previous alpha-adrenergic blockade with phentolamine. In 7 control persons NE and E levels were measured also after beta-adrenergic blockade with propranolol. The following results were obtained: 1. At rest NE levels showed no significant differences between the groups. After exercise an increase of NE was observed in all groups, but in patients, even after phentolamine, and in normals after propranolol the increase was significantly higher than in the normal group within the control test. 2. No significant differences between the groups were found in E levels at rest and after exercise. Exercise caused no significant increase of E levels, except in the normals after propranolol application. 3. No significant correlation existed between NE levels and the increase of airway resistance after exercise. It is concluded that during exercise in asthmatics the sympathetic activity is enhanced, but the provocation of an EIB does not seem to be mediated by enhanced plasma NE levels.

Adrenergic alpha-Antagonists↗
PubMed1986

The role of vagus nerve on histamine- and acetylcholine-induced bronchoconstriction (experiments on cats).

During administration of highly concentrated acetyclcholine and histamine aerosol (20-40 min), different effects on tidal volume, respiratory rate, and bronchial tone could be demonstrated. Inhalation after vagotomy neither showed changes in respiratory rate nor in tidal volume. These results point out the importance of the nervus vagus in case of bronchoconstriction caused by mediators. It is discussed to which degree vagus activity is required for the direct effect of different mediators in living animals.

Acetylcholine↗
PubMed1986

LG 30435, a new bronchodilator/antiallergic agent, inhibits PAF-acether induced platelet aggregation and bronchoconstriction.

LG 30435 is a quaternary phenothiazinic antihistamine, endowed with bronchodilator and antiallergic activity. Since PAF-acether (PAF) is a potential mediator of asthma, LG 30435 was assayed for its ability to counteract PAF-induced platelet aggregation (PA) in rabbit platelet rich plasma and bronchoconstriction (BC) in anaesthetized guinea-pigs, in comparison with other antihistamines. LG 30435 was the most potent and selective inhibitor of PAF-induced PA (IC50: 66 microM), concentrations three and more than fifteen fold higher being needed to inhibit PA induced by collagen and arachidonic acid respectively. The other antihistamines, namely mepyramine, promethazine, mequitazine, thiazinamium methyl sulfate and ketotifen were less potent inhibitors of PAF-induced PA, while interfered at lower concentrations with collagen-induced PA. LG 30435 and thiazinamium, administered intravenously, inhibited dose-dependently PAF-induced BC, starting from the dose of 0.1 mumol/kg. The ED50 of LG 30435 was 0.28 mumol/kg, while the inhibition obtained with thiazinamium did not reach 50% even at 3 mumol/kg. Ketotifen and promethazine were partially active only at 3 mumol/kg, while mequitazine and mepyramine were inactive up to this dose. These results show that LG 30435 is endowed with a peculiar anti-PAF action, which may be advantageous in the treatment of asthma.

Animals↗
PubMed1984

Leukotriene D4 potentiates histamine-induced bronchoconstriction in guinea-pigs.

Histamine concentration-response curves performed on isolated airways smooth muscle preparations were unaffected by threshold constrictor concentrations of LTD4 (194 +/- 34 pM for parenchymal strips and 1940 +/- 480 pM for isolated trachea, respectively). In contrast, LTD4, when administered between 2 and 60 s beforehand, potentiated bronchoconstrictor responses to histamine in anaesthetized, artificially ventilated guinea-pigs. Doses of LTD4, which did not produce direct effects on airways resistance, potentiated histamine-induced bronchoconstriction to a lesser degree than those having small direct effects. This potentiation was prevented by bilateral vagotomy. In addition, the antagonists atropine (100 micrograms/kg), FPL55712 (5 mg/kg) and indomethacin (1 mg/kg) effectively prevented the interaction. It is suggested that the interaction between LTD4 and histamine involves a specific leukotriene receptor, possibly linked to the generation of a cyclo-oxygenase metabolite and requires intact cholinergic innervation of airways smooth muscle. Furthermore, these results are consistent with the hypothesis that LTD4 may be a mediator of bronchial hyperreactivity.

Airway Resistance↗