Ambient nitrogen dioxide concentrations increase bronchial responsiveness in subjects with mild asthma

Twenty subjects with mild asthma were exposed at rest in a body plethysmograph, to NO2 at 0, 260, 510 and 1,000 micrograms.m3, for 30 min on four separate days. Bronchial responsiveness (histamine inhalation test) was measured after each exposure session. Airway resistance (Raw), thoracic gas volume (TGV) and specific airway resistance (sRaw) were measured before, during and after exposure, and the breathing pattern was monitored during the whole session. Bronchial responsiveness increased significantly after 30 min exposure to 510 micrograms.m3 NO2 (p less than 0.01). There were also tendencies to an increased bronchial responsiveness after exposure to 260 and 1,000 micron.m3 NO2, but these changes were not statistically significant. Effects on airway resistance and breathing pattern were not demonstrated by exposure to 0-1,000 micrograms.m3 NO2. We conclude that short-term NO2 exposure at about 500 micrograms.m3 slightly affects human bronchial responsiveness in subjects with mild asthma.     

Bronchial responsiveness to eucapnic hyperventilation and methacholine following exposure to organic dust

STUDY OBJECTIVE: Inhalation of dust in a swine confinement building causes an intense airway inflammatory reaction in the airways and increased bronchial responsiveness to methacholine. The aims of the present study were to investigate whether exposure to organic dust also influences bronchial responsiveness to an indirect stimulus, and to assess the duration of increased postexposure bronchial responsiveness. DESIGN: Twenty-two healthy nonatopic, nonsmoking subjects were exposed to dust for 3 h in a swine confinement building. Lung function was assessed, and either a methacholine bronchial provocation (n = 11) or a challenge with eucapnic hyperventilation of dry air (n = 11) was performed before exposure and at 7 h, 1 week, 2 weeks, and 4 weeks after exposure. RESULTS: Vital capacity and FEV(1) decreased 3% and 6%, respectively (p < 0.001), and airway resistance increased 15% (p < 0.05) after exposure. The median provocative dose of methacholine causing a 20% decline in FEV(1) fell from 1.38 mg (25th to 75th percentiles, 0.75 to 7.20 mg) before exposure to 0.18 mg (0.11 to 0.30 mg) after exposure (p = 0.004). Corresponding values for the dose-response slope were 15.3%/mg (2.88 to 25.3%/mg) and 100.2%/mg (2.1 to 27.3%/mg), respectively (p = 0.01). Bronchial responsiveness to eucapnic hyperventilation was not affected by the exposure: FEV(1) fell 4.3% (- 7.2 to - 1.8%) before and 4.8% (- 6.7 to - 1.6%) after exposure (p = 0.72). One week after exposure, the bronchial responsiveness to methacholine was normalized. CONCLUSIONS: The bronchial responsiveness to methacholine but not to dry air increases after exposure to swine house dust. Thus, exposure to organic dust induces increased bronchial responsiveness with different characteristics from that frequently found in asthma.     

Effects of a two-year inhalation exposure of rats to coal dust and/or diesel exhaust on tension responses of isolated airway smooth muscle

This study was performed to determine whether chronic inhalation exposure of rats to levels of coal dust (CD) and/or diesel exhaust (DE) similar to those experienced by underground miners affects the pharmacologic characteristics of the animal's airway smooth muscle. Animals were exposed for 2 yr to CD alone (2 mg/m3 of respirable particulates), DE alone (2 mg/m3 of respirable particulates), or CD and DE (CD + DE) in combination (1 mg/m3 CD plus 1 mg/m3 DE). Concentration-response relationships for tension changes induced with acetylcholine, 5-hydroxytryptamine, potassium chloride, and isoproterenol were assessed in vitro on isolated preparations of rat airway smooth muscle (trachealis). Compared with control animals, the maximal contractile responses to acetylcholine of tissues from CD-, DE-, and CD + DE-exposed animals were significantly increased; the effects of CD and DE exposure were additive. The CD + DE exposure, but not the individual treatments, resulted in a significant increase in the maximal relaxation response elicited by isoproterenol; this interaction may have resulted from the addition of, or the synergism between, the nonsignificant effects of CD and DE alone. No treatment altered the sensitivity (EC50 values) of the muscles to the agonists used. The results indicate that chronic exposure to CD, DE, and CD + DE produces differential modifications in the behavior of rat airway smooth muscle. These findings may have some bearing on humans exposed to these substances.     

The effect of platelet activating factor antagonist on ozone-induced airway inflammation and bronchial hyperresponsiveness in guinea pigs.

We investigated the role of platelet-activating factor (PAF) in ozone-induced airway responses by examining the effects of L659,989, a potent PAF antagonist, on bronchial hyperresponsiveness and airway inflammation. Twenty-four male guinea pigs were studied in four equal groups. Total lung resistance (RL) in intubated and spontaneously breathing animals was measured in a constant-volume body plethysmograph. Dose-response curves to methacholine were determined in all animals at the start of the experiment. These were repeated on a separate day after the following types of treatments: air exposure in Group 1, intraperitoneally administered alcohol and air exposure in Group 2; intraperitoneally administered alcohol and ozone exposure in Group 3, and intraperitoneally administered L659,989 (a specific PAF antagonist), 5 mg/kg dissolved in alcohol, and ozone exposure in Group 4. Bronchoalveolar lavage (BAL) was performed after the second methacholine challenge, and the bronchial mucosa was also examined for inflammatory cells. Exposure to 3 ppm ozone for 2 h resulted in a three-doubling concentration increase in bronchial responsiveness, which was not significantly inhibited by prior treatment with L659,989. Ozone induced a 1.8-fold increase in BAL total cell count, increased eosinophilic influx into the airways, and increased eosinophilic infiltration in the bronchial mucosa, which were all not inhibited by L659,989 pretreatment. The results suggest that PAF may not have an essential role in ozone-induced airway hyperresponsiveness and nonallergic airway inflammation.     

Diesel exhaust enhances airway responsiveness in asthmatic subjects.

Particulate matter (PM) pollution has been associated with negative health effects, including exacerbations of asthma following exposure to PM peaks. The aim of the present study was to investigate the effects of short-term exposure to diesel exhaust (DE) in asthmatics, by specifically addressing the effects on airway hyperresponsiveness, lung function and airway inflammation. Fourteen nonsmoking, atopic asthmatics with stable disease, on continuous treatment with inhaled corticosteroids, were included. All were hyperresponsive to methacholine. Each subject was exposed to DE (particles with a 50% cut-off aerodynamic diameter of 10 microm (PM10) 300 microg x m(-3)) and air during 1 h on two separate occasions. Lung function was measured before and immediately after the exposures. Sputum induction was performed 6 h, and methacholine inhalation test 24 h, after each exposure. Exposure to DE was associated with a significant increase in the degree of hyperresponsiveness, as compared to after air, of 0.97 doubling concentrations at 24 h after exposure (p < 0.001). DE also induced a significant increase in airway resistance (p=0.004) and in sputum levels of interleukin (IL)-6 (p=0.048). No changes were detected in sputum levels of methyl-histamine, eosinophil cationic protein, myeloperoxidase and IL-8. This study indicated that short-term exposure to diesel exhaust, equal to high ambient levels of particulate matter, is associated with adverse effects in asthmatic airways, even in the presence of inhaled corticosteroid therapy. The increase in airway responsiveness may provide an important link to epidemiological findings of exacerbations of asthma following exposure to particulate matter.     

Hypoxia enhances nonspecific bronchial reactivity

Enhancement of nonspecific bronchial reactivity has been observed after antigen-induced bronchoconstriction, a mast-cell-mediated phenomenon. Because hypoxia also causes degranulation of mast cells, we tested the hypothesis that alveolar hypoxia produces nonspecific bronchial reactivity. In 11 conscious sheep, we determined specific lung resistance (SRL) (mean pulmonary flow resistance times thoracic gas volume) before and after exposure to either air-sham or a hypoxic gas mixture (13% O2, balance N2), with and without cromolyn sodium pretreatment. The sheep then received 50 breaths of 5% histamine or 10 breaths of 2.5% carbachol on different days. Inhalation of histamine and carbachol after air-sham caused a significant increase in mean SRL to 350 and 403% of baseline, respectively (p less than 0.01). A 30-min exposure to the hypoxic gas mixture, which per se had no effect on SRL, enhanced the histamine and carbachol-induced increases in SRL to 519 and 472% of baseline (p less than 0.01). These increases were significantly greater than those observed after air-sham exposure (p less than 0.05). Infusion of cromylyn sodium (3 mg/kg/min) before and during exposure to hypoxia prevented the posthypoxia enhancement of histamine-induced (n = 7) and carbachol-induced (n = 5) bronchoconstriction, without affecting the airway responsiveness to these agents during normoxia. These data suggest that alveolar hypoxia enhances nonspecific bronchial reactivity in sheep, which may be related to hypoxia-induced release of mast-cell mediators.     

Influence of low concentrations of allergens on bronchial system

The influence of Ascaris extract, applied during 1 h in low concentration as aerosol and intravenously, on the bronchial system and the potentiation of increase of airway resistance to acetylcholine (ACH) and histamine challenge caused by this kind of allergen exposure were studied in 13 dogs. All the animals presented no reaction by the allergen exposure itself but developed an increased response to ACH and histamine after this kind of allergen exposure. A control group of 4 dogs was submitted to saline solution aerosol and intravenous application. No change in response to the substances mentioned was observed. The airway response to cold air after concentrated and diluted Ascaris suum extract (AE) aerosol application was tested on 7 dogs. The response to cold air was only influenced after concentrated AE-aerosol exposure.     

Mechanism of airway narrowing caused by inhaled platelet-activating factor. Role of airway microvascular leakage

In order to study the mechanism of airway narrowing after inhaled platelet-activating factor (PAF) we measured concomitant changes in lung resistance (RL) and in airway microvascular leakage in anesthetized guinea pigs. RL and its recovery after hyperinflation at 5 min were measured until 6 min after PAF aerosol (0.1, 0.3, 1, and 3 mM), and in the case of 3 mM PAF also until 10 min. Microvascular leakage in trachea, main bronchi, and proximal and distal intrapulmonary airways was determined by measurement of extravasated Evans blue dye content. For comparison, the responses to inhaled histamine (3 mM) and 5-hydroxytryptamine (5HT) (3 mM), which act directly on airway smooth muscle, were also examined. Inhaled PAF increased RL dose-dependently, with a maximal response (peak RL) at 4 min after the inhalation, whereas the response to histamine or 5HT was maximal within a few seconds after the inhalation. Peak RL (cm H2O/ml/s) was significantly less after PAF (1.03 +/- 0.09) than after histamine (8.39 +/- 1.07) or 5HT (18.3 +/- 6.48), although there was no significant difference in RL after hyperinflation (recovery RL). No additional increase in RL was seen between 5 and 10 min after exposure. PAF caused a dose-dependent increase in Evans blue dye extravasation; 3 mM PAF induced significantly higher leakage than did histamine or 5HT at all airway levels at 6 min. PAF did not cause any additional extravasation of Evans blue dye at 10 min compared with that at 6 min after exposure.(ABSTRACT TRUNCATED AT 250 WORDS)     

Indomethacin does not inhibit the ozone-induced increase in bronchial responsiveness in human subjects

Exposure of human subjects to sufficiently high levels of ozone can result in reversible changes in lung function (restrictive in nature) and increases in nonspecific airway responsiveness. Several studies have implicated products of cyclooxygenase metabolism in the mediation of these changes. The purpose of this study was to determine if indomethacin (a cyclooxygenase inhibitor) would alter the changes in the ozone-induced increase in responsiveness to methacholine or the ozone-induced decrease in lung function. Thirteen male subjects underwent three randomly assigned 2-h exposure to 0.4 ppm ozone with alternating 15-min periods of rest and exercise on a cycle ergometer (30 L/min/m2, body surface area). For the 4 days before each of the exposures, the subjects received either indomethacin (150 mg/day) or placebo, or no modification. Of the 13 subjects, only seven had both detectable indomethacin serum levels on the indomethacin Study Day and a significant increase in bronchial responsiveness to methacholine on the No Medication Day. For this group of seven subjects, we found that indomethacin did not alter the ozone-induced increase in bronchial responsiveness to methacholine (decrease in PC100SRaw for the different study days: no medication, -78.4 +/- 5.3% [mean +/- SEM]; placebo, -48.9 +/- 12.2%; indomethacin, -64.5 +/- 6.3%; p greater than 0.2), although indomethacin did attenuate the ozone-induced decrease in lung function. The decrease in the FEV1 for the different study days was as follows: no medication, -20.7 +/- 5.0% (mean +/- SEM); placebo, -19.2 +/- 6.3%; indomethacin, -4.8 +/- 3.7% (p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of Age on Bronchial Reactivity in Children with Asthma

In contrast to an abundance of data concerning age-related changes of bronchial sensitivity, the relationship between age and rapidity of bronchoconstriction (bronchial reactivity) remains unclear. We studied age and bronchial reactivity in children with asthma. Enrolled in this study were 511 asthmatic subjects and 115 age-matched control subjects 1 to 16 years of age. Bronchial reactivity was represented by the slope of the methacholine transcutaneous oxygen pressure dose-response curve (SPO₂) in younger children and the slope of the respiratory resistance dose-response curve (SRrs) in older children. Overall, SPO₂ and SRrs were higher in asthmatic than control subjects. SPO₂ increased significantly from 1 to 6 years in asthmatic subjects, reaching a plateau after age 7. This age-related change in SPO₂ also was seen in controls. SRrs in asthmatic subjects decreased after age 13, while SRrs in controls showed no significant change between age 7 and 16. Age-related change in bronchial reactivity occurs during childhood, possibly reflecting early changes in airway smooth muscle maturity and later changes in airway wall rigidity.     

Effects of esophageal acid perfusion on airway hyperresponsiveness in patients with bronchial asthma

STUDY OBJECTIVES: The effects of gastroesophageal reflux on airway hyperresponsiveness in patients with bronchial asthma have yet to be studied in significant detail. The purpose of the present study was to determine how esophageal acid perfusion could change airway responsiveness in patients with bronchial asthma. PATIENTS AND INTERVENTIONS: In seven patients with bronchial asthma (mean +/- SD age, 55.1 +/- 6.4 years; four women and three men), esophageal pH was monitored by a pH meter and airway responsiveness was evaluated by aerosol inhalation of methacholine, during esophageal perfusion through an esophageal tube filled with either saline solution or 0. 1N hydrochloric acid (HCl), the order of which was selected at random, in 1-week intervals. Spirometry was also performed during esophageal pH monitoring. RESULTS: A significant decrease in the geometric mean of airway sensitivity or the concentration of methacholine causing a 35% fall in respiratory conductance was observed during esophageal HCl perfusion compared with that of saline solution perfusion (p < 0.01 or p < 0.003), although no significant changes were observed in vital capacity, FEV(1), peak expiratory flow, respiratory resistance, or slope of respiratory conductance during the periods of saline solution and HCl perfusion. CONCLUSION: We concluded that an increase in airway hyperresponsiveness was induced when HCl stimulated the esophagus in patients with bronchial asthma. These results suggest that esophageal reflux is one of the important factors that aggravate asthmatic status.     

Different airway inflammatory responses in asthmatic and healthy humans exposed to diesel.

Particulate matter (PM) pollution adversely affects the airways, with asthmatic subjects thought to be especially sensitive. The authors hypothesised that exposure to diesel exhaust (DE), a major source of PM, would induce airway neutrophilia in healthy subjects, and that either these responses would be exaggerated in subjects with mild allergic asthma, or DE would exacerbate pre-existent allergic airways. Healthy and mild asthmatic subjects were exposed for 2 h to ambient levels of DE (particles with a 50% cut-off aerodynamic diameter of 10 microm (PM10) 108 microg x m(-3)) and lung function and airway inflammation were assessed. Both groups showed an increase in airway resistance of similar magnitude after DE exposure. Healthy subjects developed airway inflammation 6 h after DE exposure, with airways neutrophilia and lymphocytosis together with an increase in interleukin-8 (IL-8) protein in lavage fluid, increased IL-8 messenger ribonucleic acid expression in the bronchial mucosa and upregulation of the endothelial adhesion molecules. In asthmatic subjects, DE exposure did not induce a neutrophilic response or exacerbate their pre-existing eosinophilic airway inflammation. Epithelial staining for the cytokine IL-10 was increased after DE in the asthmatic group. Differential effects on the airways of healthy subjects and asthmatics of particles with a 50% cut-off aerodynamic diameter of 10 microm at concentrations below current World Health Organisation air quality standards have been observed in this study. Further work is required to elucidate the significance of these differential responses.     

Effect of inhaled ipratropium bromide on the airway response to methacholine, histamine, and exercise in patients with mild bronchial asthma.

We studied the bronchodilator and protective potency of inhaled ipratropium bromide in 33 patients with mild bronchial asthma. Patients were divided into 3 groups with similar baseline lung function and similar degrees of bronchial hyperresponsiveness to participate in the methacholine (study I, n = 9), histamine (study II, n = 9), or exercise challenge tests (study III, n = 18). At each session, 80 micrograms ipratropium bromide or placebo were inhaled in a double-blind randomized fashion. After ipratropium bromide, the mean specific airway resistance (SRaw) decreased from 10.4 to 4.9 (study I, p less than 0.01), 9.3 to 5.4 (study II, p less than 0.05), or 7.8 to 5.1 cm H2O.s (study III, p less than 0.01), respectively. Mean methacholine provocation concentrations necessary to increase SRaw by 100% were 0.43 after placebo and 8.60 mg/ml after ipratropium bromide (p less than 0.01), the respective values after histamine challenges were 1.32 mg/ml after placebo and 2.25 mg/ml after ipratropium bromide (p less than 0.01). In the exercise challenges, the individual responses varied largely with a mean maximum percent increase in SRaw of 231% after placebo and 173% after ipratropium bromide pretreatment (p less than 0.05). Therefore, ipratropium bromide offers bronchodilation and protection against a variety of stimuli and should more often be considered as an effective and safe drug for asthma treatment.     

Threshold concentration of ozone causing an increase in bronchial reactivity in humans and adaptation with repeated exposures

To determine the lowest concentration of ozone that causes an increase in bronchial reactivity to histamine and to determine whether adaptation to this effect of ozone develops with repeated exposures, we studied 19 healthy adult subjects. Bronchial reactivity was assessed by measuring the rise in specific airway resistance (delta SRaw) produced by inhalation of 10 breaths of histamine aerosol (1.6% solution). In 5 subjects, bronchial reactivity was determined at 9:00 and 11:30 A.M. on 4 consecutive days without exposure to ozone (Group I). In 7 other subjects (Group II), bronchial reactivity was assessed at 9:00 and 11:30 A.M. on 3 consecutive days, and subjects were exposed to 0.2 ppm of ozone from 9:30 to 11:30 A.M. on the third day. Seven additional subjects (Group III) had bronchial reactivity assessed in a similar fashion for 2 days and then again on 3 consecutive days of 2-h exposures to 0.4 ppm of ozone. Pre-exposure bronchial reactivity of the groups was the same, and no change in bronchial reactivity occurred in the group tested repeatedly but not exposed to ozone. An increase in delta SRaw provoked by histamine was noted after the first exposure to 0.4 ppm but not to 0.2 ppm of ozone (p less than 0.025). With 3 repeated 2-h exposures to 0.4 ppm on consecutive days, however, the delta SRaw produced by histamine progressively decreased, returning to pre-exposure values after the third exposure. Our results indicate that the threshold concentration of ozone causing an increase in bronchial reactivity in healthy human subjects is between 0.2 and 0.4 ppm, and that adaptation to this effect of ozone develops with repeated exposures. The threshold concentration of ozone identified in other studies as causing changes in symptoms, lung volumes, or airway resistance was also between 0.2 and 0.4 ppm, and the time course of the development of tolerance to ozone in these other studies was similar to hat observed in our study. We propose that the appearance of symptoms, changes in pulmonary function, and the increase in bronchial reactivity may be caused by a change in the activity of afferent nerve endings in the airway epithelium.     

A trial of inhaled budesonide on airway responsiveness in smokers with chronic bronchitis

The aim of the present randomized, double-blind study was to evaluate the effect of inhaled budesonide on daily symptoms, ventilatory capacity, and airway responsiveness in smokers with chronic bronchitis. Twenty-five subjects with a provocative concentration producing a 20% fall in forced expiratory volume in one second PC20(FEV1) less than 2.0 mg.ml-1, by bronchial histamine challenge, were included. Eighteen subjects accomplished the entire 12 week study, eight receiving inhaled budesonide 400 micrograms b.i.d. and ten receiving placebo. Cough decreased significantly in the actively treated group during the treatment period, but no change could be demonstrated in expectoration, dyspnoea, or sleep disturbances. No changes in any of these symptoms were found in the placebo group, and no differences in symptoms scores were found between the groups. No significant differences in ventilatory capacity or bronchial responsiveness could be demonstrated. In conclusion, a moderately high dose of inhaled steroid in eight subjects with chronic bronchitis did not improve the symptom scores, ventilatory capacity, or airway responsiveness to any clinically relevant degree.     

Effects of inhaled steroids on methacholine-induced bronchoconstriction and gas trapping in mild asthma.

According to a recent hypothesis, airway smooth muscle regulates airway calibre mostly at high lung volume, whereas the mucosa and adventitia dimensions dominate at low lung volumes. It was thought that if inhaled steroids decrease the thickness of airway wall in asthma, then forced vital capacity (FVC), which reflects the functional changes at low lung volume, should decrease less during induced bronchoconstriction than flow at high volume. The study was conducted in 31 mild asthmatics under control conditions and during a methacholine challenge before and after 4-weeks treatment with inhaled fluticasone dipropionate (1.5 mg daily, 16 patients) or placebo (15 patients). After fluticasone dipropionate treatment, control forced expiratory volume in one second (FEV1), and maximal flow at 50% of control FVC during forced expiration after a maximal (V'max,50) and a partial inspiration (V'p,50) significantly increased. During methacholine challenge, FVC decreased less than did FEV1 or V'max,50, and so did inspiratory vital capacity compared to V'p,50. Both the provocative dose of methacholine causing a 20% fall in FEV1 and the bronchodilator effect of deep inhalation significantly increased. The latter was assessed by means of the regression coefficient of all V'max,50 plotted against V'p,50. No significant changes in these parameters occurred after placebo. These data show that inhaled steroids remarkably blunt the occurrence of gas trapping during induced bronchoconstriction in mild bronchial asthma, possibly due to their effect on airway wall remodelling.     

The effect of inhaled naloxone on resting bronchial tone and exercise-induced asthma

We wanted to determine whether 10 mg naloxone inhaled quantitatively could modulate the resting bronchial tone and respiratory response in exercise-induced asthma (EIA). In 11 asthmatic subjects, we measured specific airway conductance (SGaw) and forced expiratory flow (FEF) before and after the inhalation of naloxone or saline. In another 10 asthmatic subjects, we measured SGaw, FEF, and the ventilatory gas exchange, heart rate, and blood pressure responses produced by a treadmill exercise during 3 separate days: without any pretreatment (Day 1) or preceded by the inhalation of either 10 mg naloxone (Day 2) or saline (Day 3). We found that after 10 mg inhaled naloxone only one of 11 subjects bronchodilated, displaying an isolated, reproducible delta SGaw greater than 40% at 30 and 60 min. In the EIA protocol, the cardiopulmonary responses during exercise remained similar on all experimental days, but in seven of 10 subjects (all with %FEV1/FVC greater than or equal to 70% delta SGaw was -60 +/- 11%, + 1 +/- 40%, and -52 +/- 7% during no treatment, naloxone, and saline days, respectively (p less than 0.05). FEF changes were comparable on all days (p greater than 0.05). In conclusion: (1) consistent with the general role of endogenous opioids, these neurotransmitter/neuromodulators can modulate a stress-related bronchoconstrictor response (EIA), but only very seldom the resting bronchial tone. (2) Naloxone does not blunt EIA through a decrease in the asthmogenic stimulus (i.e., ventilation) or airway caliber change, but presumably through competition with the endogenous opioids released during exercise.     

Inhalative Noxen: Schwefeldioxyd

SO₂ shows different reactions on the lung and on the bronchial tree, depending on concentration and on duration of exposure. Low concentration can increase the sensitivity of the bronchial receptors, higher concentrations can directly increase the airway resistance. This reaction depends also on other particles inhaled at the same time. Coal dust (8 mg/m³) has no influence on the SO₂ effect. Higher concentrations can cause chronic obstructive bronchitis, as could be shown in dogs. Persons exposed to SO₂ at work should be checked for the reaction of their bronchial systems.     

脉冲振荡肺功能(IOS)评价临床控制的支气管哮喘患者外周气道功能状态

目的探讨达到临床控制及部分控制的支气管哮喘患者在支气管舒张试验前后的外周气道功能状态。方法采用前瞻性研究方法,对我院60例已明确诊断为支气管哮喘患者经规范化诊治3月后行哮喘控制测试(ACT)评分、行脉冲振荡肺功能检测(IOS)气道阻力及常规通气功能后给予沙丁胺醇气雾剂200μg吸入,15 min后再次测定气道阻力及常规通气功能。同时选择30例对照者行气道阻力及常规通气功能检测。了解我院支气管哮喘患者控制情况,支气管舒张试验阳性率情况,并观察支气管舒张前后气道阻力及通气功能变化及其相关性。结果 (1)我院哮喘规范化治疗3月后临床控制率为56.9%;(2)临床控制哮喘患者支气管舒张试验阳性率为12.1%,部分控制组支气管舒张试验阳性率为45%;(3)与对照组相比,哮喘控制组及部分控制组外周气道阻力仍明显升高,控制组中心气道阻力与对照组差异无统计学意义,支气管舒张试验后外周气道阻力下降幅度大于中心气道阻力,结论 (1)支气管哮喘规范化诊治后临床控制率为24.5%;(2)支气管哮喘临床控制后仍存在气道高反应性;(3)即使在控制水平的支气管哮喘患者,仍存在外周气道阻力升高,且随着控制水平的降低而加重。IOS可用于评估哮喘外周气道功能状态。