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PubMed1995

Angiotensin II potentiates methacholine-induced bronchoconstriction in human airway both in vitro and in vivo.

Angiotensin II levels are elevated in patients with acute severe asthma. In addition, intravenous angiotensin II causes bronchoconstriction in mild asthmatic patients. In the present study, we examined the effects of this hormone on bronchi in vitro and its interaction with the cholinergic agonist methacholine both in vivo and in vitro. Contractions of rings of human bronchi were measured isometrically. Concentration-response curves were obtained to angiotensin II and to methacholine in the presence and absence of angiotensin II. In addition, seven asthmatic patients with mild bronchial hyperreactivity to methacholine received placebo, angiotensin II, 1 or 2 ng.kg-1.min, by infusion, followed by methacholine challenge. Forced expiratory volume in one second (FEV1) values were measured at baseline, at the end of the infusion and during methacholine challenge. Angiotensin II alone in vitro evoked small contractions of human bronchi ( < 0.25 g wt). Pre-incubation with low concentrations of angiotensin II significantly enhanced contractions to methacholine. In mild asthmatic patients, angiotensin II alone evoked no change in baseline FEV1 values at the levels studied. Compared to placebo, angiotensin II 2 ng.kg-1.min, but not 1 ng.kg-1.min, evoked a significant increase in bronchial reactivity to methacholine. Angiotensin II in subthreshold concentrations enhances methacholine-evoked bronchoconstrictions both in human in vitro and in mild asthmatic patients in vivo. Our findings suggest a novel role for angiotensin II as a putative mediator in asthma.

Adult↗

PubMed1998

Effect of nitric oxide synthase inhibitor on allergen- and hyperventilation-induced bronchoconstriction in guinea-pigs.

To elucidate the role of endogenous nitric oxide (NO) in allergen- (AIB) and hyperventilation-induced bronchoconstriction (HIB), the effects of an NO synthase inhibitor, NG-nitro-L-arginine methyl ester (L-NAME), on AIB and HIB were studied in guinea-pigs. In the AIB group, 21 anaesthetized guinea-pigs, actively sensitized with 1% ovalbumin, were challenged with aerosolized 0.1% ovalbumin solution under mechanical ventilation. In the HIB group, 14 guinea-pigs were challenged with hyperventilation (tidal volume of 12 mL x kg(-1) at 150 breaths x min(-1) with 21% O2 and 5% CO2 dry gas) for 5 min. In both groups, lung resistance (RL) was measured using a pressure-volume-sensitive body plethysmograph, with or without L-NAME pretreatment (8 mg x kg(-1) i.v. followed by 2 mg x kg(-1) x min(-1) i.v.). The NO precursor, L-arginine was injected at a rate of 15 mg x kg(-1) x min(-1) after L-NAME injection (10 mg x kg(-1)) in the AIB group. The results were as follows. In the AIB group, the maximal RL change was significantly potentiated by pretreatment with L-NAME. This potentiating effect of L-NAME was reversed by L-arginine. In the HIB group, the pretreatment with L-NAME had no effect on increases in RL. These findings suggest that endogenous nitric oxide may play an important role in the modulation of allergen-, but not hyperventilation-induced bronchoconstriction in guinea-pigs.

Airway Resistance↗

PubMed2007

Intravenous lidocaine after tracheal intubation mitigates bronchoconstriction in patients with asthma.

BACKGROUND: Although prophylactic IV administration of lidocaine attenuates the response to a variety of inhalation challenges, its effect on airway resistance after endotracheal intubation in patients with asthma is unclear. We tested the hypothesis that IV lidocaine attenuates intubation-evoked bronchoconstriction in patients with asthma. METHODS: Thirty patients with asthma (age 49.1 +/- 15.6 yr [mean +/- sd]) undergoing intubation after standardized anesthetic induction (etomidate 0.3 mg/kg, fentanyl 5 microg/kg, rocuronium 0.6 mg/kg, 50% nitrous oxide) were studied. Airway resistance was measured immediately after intubation and 5, 10, and 15 min later. Five minutes after intubation, either lidocaine (2 mg/kg IV for 5 min, followed by 3 mg x kg(-1) x h(-1) for 10 min) or saline was administered. RESULTS: Airway resistance immediately after intubation averaged 23 +/- 12 cm H2O x s x L(-1). Airway resistance further increased (+38%) after administration of saline, but decreased (-26%, P < 0.004) to less than the initial values after lidocaine. CONCLUSIONS: IV lidocaine given after endotracheal intubation mitigates bronchoconstriction in patients with asthma.

Adult↗

PubMed1995

[Effect of KW-4679, a novel antiallergic drug, on platelet-activating factor (PAF)-induced bronchoconstriction, airway hyperresponsiveness and pulmonary cell accumulation in guinea pigs].

We assessed the effects of KW-4679 on bronchoconstriction, airway hyperresponsiveness and infiltration of inflammatory cells into the bronchoalveolar lavage (BAL) fluid induced by platelet-activating factor (PAF) in guinea pigs. (1) KW-4679 (1, 10 mg/kg, p.o.) significantly inhibited PAF-induced bronchoconstriction in anesthetized, ventilated guinea pigs. Ketotifen (1, 10 mg/kg, p.o.) also significantly inhibited that reaction. (2) Intravenous administration of PAF (600 ng/kg/hr) to ventilated anesthetized guinea pigs induced bronchial hyperresponsiveness to histamine or substance P. PAF-induced bronchial hyperresponsiveness was significantly attenuated by pretreatment with KW-4679 (3 mg/kg, i.v.). (3) Exposure of guinea pigs to an aerosol of PAF induced an increase in the numbers of total leukocytes, eosinophils, neutrophils and lymphocytes in BAL fluid at 24 hr. KW-4679 (10 mg/kg, p.o.) reduced the increase in eosinophils in BAL fluid. Ketotifen (10 mg/kg, p.o.) partially reduced the increase in eosinophils in BAL fluid. (4) KW-4679 did not inhibit PAF-induced rabbit platelet aggregation. These observations indicate that KW-4679 attenuates the PAF-induced pulmonary reactions in guinea pigs and that these actions may be beneficial for the treatment of allergic bronchial asthma.

Animals↗

PubMed1991

Inhaled verapamil-induced bronchoconstriction in mild asthma.

Methacholine challenges were performed in ten subjects with mild asthma at 2 h before and 20 min after placebo or 5, 10, 20, 40, 80, and 160 mg of inhaled verapamil given in a single-blind randomized crossover manner on different days. While verapamil did not have a bronchodilator effect, the 10-mg dose modestly increased the concentration of methacholine required to decrease FEV1 by 20 percent (PC20). The mean (+/- SEM) increase in PC20 from baseline was 2.1 +/- 0.2 times baseline after 10 mg of verapamil, compared to 1.1 +/- 0.1 times baseline after placebo (p less than 0.001). Unexpectedly, bronchoconstriction (greater than 10 percent decrease in FEV1) associated with cough or wheezing was observed in seven of ten subjects at doses of 20 mg or more. This adverse effect was not related to the osmolarity of the nebulized solutions. Thirty minutes before a standardized exercise challenge, 13 subjects inhaled placebo, 10 mg, or the highest dose of verapamil tolerated during the methacholine study (20 to 160 mg) in a double-blind randomized crossover manner. The exercise challenge was aborted in three subjects because of bronchospasm that occurred after administration of the higher dose. The mean (+/- SEM) maximum change in FEV1 after exercise in the ten subjects completing all three regimens of treatment was -17.1 +/- 4.0 percent after placebo, -12.7 +/- 4.3 percent after 10 mg (p less than 0.05), and -6.4 +/- 3.6 percent after the highest dose (p less than 0.05). We conclude that increasing the dose of verapamil above 10 mg did not provide greater benefit but, paradoxically, induced bronchoconstriction in most of the subjects. Because of this potential bronchoconstrictor effect, high doses of oral or intravenous verapamil should be used with caution in asthmatic subjects.

Administration, Inhalation↗

PubMed1991

Aerosol pentamidine-induced bronchoconstriction. Predictive factors and preventive therapy.

OBJECTIVE: To describe the frequency of aerosol pentamidine-induced bronchoconstriction, its relationship to non-specific airway responsiveness, and its response to preventive therapy using salbutamol, ipratropium bromide, or sodium cromoglycate. METHODS: Consecutive HIV-infected individuals starting prophylactic AP were eligible if they had not been previously treated with this agent. Simple spirometry was performed before and 10 min after a single 60-mg dose given through an ultrasonic nebulizer. Methacholine challenge was performed in all subjects 24 h to four days after the initial AP dose. Subjects with a change in FEV1 (delta FEV1) greater than or equal to 10 percent decrease after the initial AP dose were restudied on three separate occasions (greater than 24 hours apart) after premedication with two puffs of salbutamol (200 micrograms), ipratropium bromide (40 micrograms), or sodium cromoglycate (2 mg), in random order. RESULTS: Fifty-three subjects were studied. The median delta FEV1 after a single dose of AP was -7.0 percent (range: -47 percent, 1.8 percent). The delta FEV1 following AP was only partially predicted by the degree of nonspecific bronchial responsiveness as measured by a standard methacholine challenge. Age, current smoking, history of asthma, baseline FEV1, or a prior episode of PCP failed to predict the delta FEV1 following AP. Eighteen subjects (34 percent) had a delta FEV1 greater than or equal to 10 percent decrease (median: -17.0 percent). In these subjects, after premedication with salbutamol, ipratropium bromide, and sodium cromoglycate, the median delta FEV1 was 1.0, 0.8, and -9.6 percent, respectively. CONCLUSION: Aerosol pentamidine produced a decrease in FEV1 greater than or equal to 10 percent in 34 percent of subjects. This was not accurately predicted by the methacholine response. The bronchoconstriction induced by AP was effectively prevented by either salbutamol or ipratropium, whereas cromoglycate was only partially effective.

Adult↗

PubMed1994

Inhaled ICI 204,219 blocks antigen-induced bronchoconstriction in subjects with bronchial asthma.

Three inhalation formulations of ICI 204,219 were compared for antagonism of antigen-induced bronchoconstriction in 16 subjects with asthma who demonstrated reproducible hypersensitivity to allergen during screening challenges. Each subject received a single 0.2-mg dose of each formulation and was challenged with ragweed 30 min after administration of ICI 204,219 until the forced expiratory volume in 1 s (FEV1) decreased by 20 percent or the maximum allergen concentration (100 micrograms/ml) was reached. The majority of subjects tolerated 100 micrograms/ml of allergen without a 20 percent decrease in FEV1. Inhalation formulations of ICI 204,219 successfully inhibited bronchoconstriction in subjects with reproducible sensitivity to ragweed challenges.

Administration, Inhalation↗

PubMed1994

Perception scoring of induced bronchoconstriction as an index of awareness of asthma symptoms.

Perception of asthma symptoms shows a wide interindividual variability. Poor perception of airflow obstruction may lead to undertreatment of asthma. We reviewed the possibility of using a simple test to detect poor perceivers of bronchoconstriction as part of the investigation of asthmat. We studied 150 consecutive subjects referred for assessment of airway responsiveness. All had a histamine PC20 within the asthmatic range (< 16 mg/ml) and a fall in FEV1 of < 20 percent after saline inhalation. On histamine challenge, before each FEV1 measurement, perception of dyspnea was assessed on a modified Borg scale. A perception score of breathlessness at 20 percent fall in FEV1 (PS20) was obtained by interpolation of the two last points on the perception/fall in FEV1 curve. It was concluded that in a hyperreactive population, PS20 (1) showed a normal distribution pattern; (2) was similar in both genders; and (3) increased with age due to high postcontrol saline inhalation scores. Hypoperceivers or hyperperceivers were similar for age, sex, baseline FEV1, and PC20. The PS20 determination may be a useful additional parameter to obtain during provocation tests to assess perception of symptoms associated with bronchoconstriction. Its correlation with clinical outcome remains, however, to be determined.

Adolescent↗

PubMed1996

Effect of inhaled salmeterol on sulfur dioxide-induced bronchoconstriction in asthmatic subjects.

UNLABELLED: This study tested the capability of a single 42-microgram dose of inhaled salmeterol xinafoate, a long-acting beta 2-agonist, to protect against bronchoconstrictive effects of exposure to 0.75 ppm sulfur dioxide (SO2) during exercise, for up to 24 h. Ten SO2-responsive adult volunteers with stable asthma were studied under 4 conditions of drug pretreatment/exposure, administered in random order, double-blind: salmeterol/SO2, placebo/SO2, salmeterol/clean air, and placebo/clean air. Each subject underwent 10-min exposure/exercise challenges in a chamber 1, 12, 18, and 24 h after pretreatment. Exercise ventilation rates averaged 29 L/min. Response was measured as the decrement in FEV1 between preexposure and postexposure (lowest value within 30 min). After salmeterol, mean decrement post-SO2 was 7% at 1 h and 12% at 12 h. At 18 and 24 h after salmeterol, and at all times after placebo, mean decrements were 25 to 30%. After 18 and 24 h, salmeterol still improved base-line FEV1 relative to placebo, although improvement was not statistically significant at 24 h. Acute symptom increases accompanied FEV1 decrements. CONCLUSION: In our asthmatic subjects, pretreatment with salmeterol imparted clinically and statistically significant (p < 0.01) protection against bronchoconstriction induced by SO2/exercise for at least 12 h, and maintained an improvement in lung function for as much as 18 h.

Administration, Inhalation↗

PubMed1997

Pharmacology of leukotriene receptor antagonists. More than inhibitors of bronchoconstriction.

The cysteinyl leukotrienes (LTs) are chemical mediators that are thought to contribute to the pathophysiologic condition of asthma and other inflammatory diseases. The biological effects of the cysteinyl LTs in the lung are pleiotropic, including both bronchoconstrictor and a growing list of nonbronchoconstrictor activities that extend to inflammatory cell recruitment, vascular leakage, mucus production, neuronal dysfunction, and airways remodeling. This spectrum of effects of cysteinyl LTs is consistent with an expanded view of asthma that extends beyond simply bronchoconstriction and inflammation. Consequently, the clinical efficacy of cysteinyl LT receptor antagonists (LTRAs) in asthma may be related to antagonism of more than cysteinyl LT-induced bronchoconstriction. The relationship of antagonism of the multiple effects of cysteinyl LTs by cysteinyl LTRAs to their utility in the therapy of asthma is addressed, and the preclinical and clinical pharmacology of cysteinyl LTRAs is reviewed.

Animals↗

PubMed1997

Effect of inhaled magnesium sulfate on sodium metabisulfite-induced bronchoconstriction in asthma.

BACKGROUND: Inhaled magnesium (Mg) seemed to have a mild protective (nonbronchodilator) effect against histamine and methacholine. Inhaled sodium metabisulfite (MBS) causes bronchoconstriction in asthma through indirect mechanisms that involve sensory nerve stimulation, and it is extensively used to study airway hyperresponsiveness. We designed this double-blind, randomized, crossover, and placebo-controlled study to test the effect of nebulized Mg sulfate against indirect challenge with MBS. METHODS: Ten asthmatic subjects (three male) aged 38.8 (3.29, SEM) years came on three occasions to perform MBS challenges 5 min after inhalation of either normal saline solution as placebo or Mg sulfate (4 mL; 286 mOsm). Doubling increasing concentrations of MBS were administered by continuous nebulization at tidal breathing during 1 min starting at 0.3 to 80 mg/mL until a >20% fall in FEV1 (PC20) from post saline solution baseline value was achieved. PC20 values were logarithmically transformed before analysis. RESULTS: The mean baseline FEV1 at control day was 2.52 (0.14) L and 88.46 (4.28) percentage predicted, while the geometric mean MBS PC20 was 1.95 (1.38, geometric SEM) mg/mL. After placebo, the geometric mean PC20 was 2.26 (1.26) mg/mL. Inhaled Mg increased significantly the PC20 to 5.06 (1.52) mg/mL; p<0.05. Mg diminished the bronchoconstrictor response to MBS by 1.3 doubling doses (p=0.08). CONCLUSIONS: Inhaled Mg attenuates MBS-induced bronchoconstriction in these asthmatic subjects. This new feature of Mg, even modest in magnitude, emphasizes the necessity of studying the potential role of this cation in modulating airway response.

Administration, Inhalation↗

PubMed2005

Identification and treatment of bronchoconstriction induced by a vagus nerve stimulator employed for management of seizure disorder.

We evaluated a 63-year-old woman who developed dyspnea with a sensation of chest tightness that was temporally associated with discharges from a vagus nerve stimulator that had been implanted for the control of intractable seizures. Spirometry demonstrated the development of significant airflow obstruction associated with the firing of the stimulator. Adjustment of the stimulator settings resolved the discharge-associated bronchoconstrictive phenomenon. These findings highlight an important association between vagus nerve stimulators and dyspnea that should be considered in the differential diagnosis of patients with these devices who present with dyspnea and/or chest tightness. The relative importance of vagal stimulation to bronchoconstriction is suggested by the findings.

Bronchoconstriction↗

PubMed2006

Dynamic hyperinflation during bronchoconstriction in asthma: implications for symptom perception.

OBJECTIVE: The objective of this study was to examine the relationship between respiratory symptom intensity and quality and dynamic lung hyperinflation (DH) during induced bronchoconstriction in asthma. PATIENTS AND METHODS: Subjects with asthma (n = 116) underwent baseline spirometry and lung volume measurement followed by high-dose methacholine challenge testing (MCT) [maximum decrease in FEV(1) of 50% from baseline]. Dyspnea intensity (Borg scale) was measured after each dose of methacholine. Qualitative descriptors of breathlessness and functional residual capacity (FRC) were measured at the doses nearest to the provocative concentration of methacholine causing a 20% fall in FEV (PC(20)) and at the highest dose of methacholine (maximum response). RESULTS: FEV(1) decreased by 24.7 +/- 0.7% (mean +/- SEM) at the dose nearest to PC(20) and by 46.1 +/- 1.1% at maximum response. Inspiratory capacity decreased by 0.62 +/- 0.04 L at the dose nearest to PC(20) and 1.06 +/- 0.06 L at maximum response. The descriptor clusters "inspiratory difficulty," "chest tightness," "unsatisfied inspiration," and "work" were selected at the dose nearest to PC(20) but were more frequently selected at maximum response (p < 0.0001). Individuals who reported chest tightness at maximum response had greater airflow obstruction and higher FRC (percentage of predicted) than those who did not report chest tightness. CONCLUSIONS: Four dominant qualities of dyspnea in asthma (inspiratory difficulty, chest tightness, unsatisfied inspiration, and work) were reported early in the course of MCT and evolved in parallel, becoming more prevalent at maximum response. Significant DH accompanied even mild bronchoconstriction during MCT in asthma, making it difficult to separate mechanisms of chest tightness from other dominant respiratory sensations.

Adult↗

PubMed1991

Effects of PAF antagonist, BN52021, on the PAF-, methacholine-, and allergen-induced bronchoconstriction in asthmatic children.

Platelet-activating factor (PAF) is an inflammatory mediator capable of inducing protracted inflammation of the airways and bronchial hyperreactivity. Twenty-one asthmatic children were evenly divided into three groups and each group performed a double-blind, placebo-controlled and crossover study on the effect of aerosolized BN52021, a PAF antagonist, on the bronchoconstriction induced by PAF, methacholine, or specific allergen, respectively. One group of healthy children was included for comparison. Total WBC, neutrophils, and eosinophils were counted before and after PAF challenge. The results showed the following: (1) six of seven asthmatics and one of seven normal subjects gave a positive bronchial provocation with PAF; (2) in asthmatics, prior inhalation of BN52021 could inhibit the bronchoconstriction induced by PAF (6/6) and allergen (3/7), but not by methacholine; and (3) 5 min after inhalation of PAF, there was a marked decrease of peripheral blood eosinophils and neutrophils that could be inhibited by prior inhalation of BN52021 in normal subjects but not in asthmatics. These findings support the idea that PAF may be involved in the pathogenesis of bronchial asthma and PAF antagonist may have a role in the prevention and treatment of this disease.

Allergens↗

PubMed2006

Role of acetylcholine and muscarinic receptors in serotonin-induced bronchoconstriction in the mouse.

For the murine trachea, it has been reported that constriction evoked by serotonin (5-HT) is largely dependent on acetylcholine (ACh) released from the epithelium, owing to the sensitivity of the 5-HT response to epithelium removal, sensitivity to atropine, and insensitivity to tetrodotoxin (Moffatt et al., 2003). Consistent with this assumption, the respiratory epithelium contains ACh, its synthesizing enzyme, and the high-affinity choline transporter CHT1 (Reinheimer et al., 1996; Pfeil et al., 2003; Proskocil et al., 2004). Recently, we demonstrated that ACh can be released from non-neuronal cells by corticosteroid-sensitive polyspecific organic cation transporters (OCTs), which are also expressed by airway epithelial cells (Lips et al., 2005). Hence, we proposed that 5-HT evokes release of ACh from epithelial cells via OCTs and that this epithelial-derived ACh induces bronchoconstriction. We tested this hypothesis in a well-established model of videomorphometric analysis of bronchial diameter in precision-cut murine lung slices utilizing epithelium removal to assess the role of the epithelium, OCT mouse knockout (KO) strains to assess the role of OCT isoforms, and muscarinic receptor M2/M3 double-KO mice to assess the cholinergic component of 5-HT induced bronchoconstriction, as bronchi of this strain are entirely unresponsive to cholinergic stimulation(Struckmann et al., 2003).

Acetylcholine↗

PubMed1992

Eucapnic hyperventilation-induced bronchoconstriction in rabbits.

We examined whether eucapnic hyperventilation with dry air produces the bronchoconstriction in anesthetized, non-sensitized rabbits and in ovalbumin sensitized rabbits. Eucapnic hyperventilation challenge with dry air containing 5% CO2 at room temperature was performed with 4 non-sensitized and 7 sensitized rabbits by mechanical ventilation for 15 min (120 breaths/min, 7 ml tidal volume/kg body weight). Total lung resistance (RL) and dynamic compliance (Cdyn) were measured before and 0, 5, 15, and 30 min after hyperventilation. In non-sensitized rabbits, RL and Cdyn did not change significantly. However, in sensitized rabbits, RL increased maximally by 48.9% +/- 9.0% at 5 min, and then decreased to the baseline level at 30 min after challenge. Cdyn decreased maximally by 12.5% +/- 3.5% at 15 min after challenge. These changes were significantly different from the baselines (p < 0.05). Furthermore, to investigate the role of histamine on hyperventilation-induced bronchoconstriction (HIB) in sensitized rabbits, we performed the hyperventilation challenges in 5 sensitized rabbits with the pretreatment of H1-receptor antagonist (chlorpheniramine, 1 mg/kg, i.v.) and found that the maximum increment of RL was suppressed to 24.2% +/- 7.4% of the control, which was significantly lower than the maximal RL in nontreated sensitized rabbits (p < 0.05). We concluded that HIB occurs only in sensitized rabbits and that histamine may play an important role in the development of HIB in sensitized rabbits.

Airway Resistance↗

PubMed2001

Acute changes in bronchoconstriction influences exhaled nitric oxide level.

In previous studies the exhaled nitric oxide (NO) level of asthma patients was investigated only in association with bronchial inflammation, and whether the degree of bronchoconstriction itself influences the exhaled NO level has never been investigated. We therefore evaluated the effect of inhalation of a bronchoconstrictor (methacholine) or a bronchodilator (salbutamol) on the exhaled NO level of healthy volunteers and asthma patients. The exhaled NO level of the healthy volunteers decreased after methacholine inhalation. The exhaled NO level of patients with mild or moderate persistent asthma, who had no asthma attacks on the day of measurement, increased after salbutamol inhalation, and the exhaled NO level of asthma patients during asthma attacks increased after salbutamol inhalation followed by intravenous drip infusion of aminophylline. It is suspected that large amounts of NO are trapped in the lung distal to the constricted airway, contributing little to the exhaled NO level at the mouth. However, we expect that the trapped NO is exhaled at a larger fraction after the dilatation of the constricted small airway, thereby increasing the exhaled NO level at the mouth. In conclusion, the results of this study suggest that acute changes in bronchoconstriction themselves influence the exhaled NO level independently of the change in NO synthase activity associated with airway inflammation.

Adult↗

PubMed1989

Bronchoconstrictive effect of ultrasonic nebulized distilled water on asthmatic children.

We studied the airway responsiveness of asthmatic and normal children to ultrasonic nebulized distilled water (UNDW inhalation test). It was found that this stimulus induced a fall in FEV1 (forced expiratory volume in 1 s) in asthmatic children, but little fall in normal children. This airway response was shown to be reproducible at about 2-week intervals. The more severe the asthma, the higher the percentage of the responders to the UNDW inhalation test, and the greater the fall in FEV1. The results of the UNDW inhalation test did not correlate with that of acetylcholine inhalation test or of exercise-induced asthma (EIA). UNDW-induced bronchoconstriction was inhibited by premedication with disodium cromoglycate (DSCG) (20 mg) or inhaled ipratropium bromide (40 micrograms). Jet-nebulized distilled water induced little fall in FEV1 in asthmatic children. These data suggest that UNDW-induced bronchoconstriction may involve the release of chemical mediators from the mast cells and cholinergic pathways. We conclude that UNDW inhalation test is a safe, less burdensome, and rather convenient method to evaluate clinically nonspecific airway hyperresponsiveness in asthmatic children.

Acetylcholine↗