吸入一氧化氮与沙丁胺醇对哮喘患者肺功能的影响

为探讨吸入一氧化氮（ＮＯ）与吸入沙丁胺醇（Ｖｅｎｔｏｌｉｎ）对支气管哮喘患者肺功能的影响。９例哮喘患者（其中组织胺激发试验阳性者５例）先后吸入２００～４００μｇ的Ｖｅｎｔｏｌｉｎ及１０ｐｐｍＮＯ观察吸入后通气功能的变化，结果显示，吸入Ｖｅｎｔｏｌｉｎ可使患者ＦＶＣ，ＦＥＶ１，ＦＥＶ１／ＦＶＣ，ＰＥＦ，ＭＭＥＦ，Ｖ５０得到明显改善；吸入ＮＯ后患者ＦＶＣ，ＦＥＶ１，ＰＥＦ明显增量ＦＥＶ１的增加幅度不及     

二丙酸倍氯米松干粉剂治疗晚发老年哮喘的临床观察

目的 观察吸入类固醇二丙酸倍氯米松（ＤＢＰ）干粉剂对晚发老年哮喘（ＬＯＡ）的疗效。方法 将２２例ＬＯＡ患者与２３例非老年２哮喘患者进行对比研究,观察吸入β２受体激动剂沙丁胺醇干粉剂后１秒钟用力呼气容积（ＦＥＶ１）的变化以及吸入ＤＢＰ干粉剂后ＦＥＶ１及其占预计值百分比（ＦＥＶ１％）、早晚最大呼气流速（ＰＥＦＲ）及其日内变异率等变化。结果 两组患者在吸入沙丁胺醇干粉剂后ＦＥＶ１均明显增高（Ｐ〈０．０１     

外源性一氧化氮及氦—氧混合气对支气管哮喘患者通气功能的影响

目的 探讨同时吸入氦－氧混合气和不同浓度的一氧化氮（ＮＯ）对支气管哮喘患者通气功能的影响。方法 选取１８例哮喘患者随机分为两组,一组吸入氦－氧混合气的同时加入１００ｐｐｍ的ＮＯ,另一组则加入４０ｐｐｍ的ＮＯ。在不同时间检测患者的通气功能,并与吸入β２受体激动剂进行比较。结果 哮喘患者吸入氦－氧混合气后与呼吸空气比较其用力肺活量（ＦＶＣ）、１秒钟用于呼气容积（ＦＥＶ１）、呼气流速峰值（ＰＥＦＲ）和最     

以肺功能实测值做为支气管激发试验的判定指标比较分析

将ＰＤ＿（２５）－Ｖ＿（５０）做为支气管激发试验的判定指标，与ＰＤ＿（２０）－ＦＥＶ＿１比较分析，两者呈高度显著直线相关。做为支气管哮喘的诊断参考指标，ＰＤ＿（２５）－Ｖ＿（５０）比ＰＤ＿（２０）－ＦＥＶ＿１更为敏感。其特异性及阳性率高，假阳性及假阴性率较４氏。以ＰＤ＿（２５）－Ｖ＿（５０）做为判定指标，可缩短支气管激发试验过程，减少吸入组织胺的累积量，避免其不良反应出现。     

吸入糖皮质激素治疗非哮喘性慢性阻塞性疾病的研究

目的 研究中等剂量二丙酸氯地米松（ＢＤＰ）短疗程吸入治疗非哮喘慢性阻塞性肺疾病（ＣＯＰＤ）是否有疗效，方法 按照随机，对照，单盲的设计，６１例非哮喘性ＣＯＰＤ患分两组，分别予ＢＤＰ（１０００μｇ．ｄ＾－１）与安慰剂吸入治疗６周，治疗前后测定肺功能一秒钟用力呼气容积（ＦＥＶ１）用力肺活量（ＦＶＣ），最大呼气中段流速（ＭＭＥＦ）值和血浆内纱（ＥＴ－１）的浓度，并记录临床症状记分，生活质量记分，结果     

雾化吸入爱喘乐对慢性阻塞性肺疾病患者肺功能的影响

为了观察雾化吸入爱喘乐（溴化异丙托品）对慢性阻塞性肺疾病（ＣＯＰＤ）患者肺功能，尤其是气道阻力的影响，对４０例ＣＯＰＤ患者随机分为雾化吸入溴化异丙托品组和吸入生理盐水组，雾化吸入前，二组临床资料和各项肺功能指标均大致相同（Ｐ＞００５）。结果：雾化吸入溴化异丙托品（０．０２５％２ｍｌ）者６０分钟后各项肺功能指标（ＦＶＣ、ＦＥＶ１、ＦＥＦ２５％～７５％、ＰＥＦＲ）均有不同程度的改善（Ｐ＜００５～００１），尤其是气道阻力（Ｒａｗ、Ｇａｗ、ｓＲａｗ、ｓＧａｗ）明显降低（Ｐ＜００１）。吸入生理盐水组各项肺功能指标均无改变（Ｐ＞００５）。     

吸入呋塞米对急性发作期支气管哮喘患者肺通气功能的影响

目的 探讨吸入呋塞米对急性发作期支气管哮喘（哮喘）患者肺通气功能的影响。方法 将６例经、中度发作期哮喘患者随机分为Ａ、Ｂ、Ｃ三组,每组各２０例。Ａ组吸入生理盐水５ｍｌ,Ｂ组吸入呋塞米５０ｍｇ（５ｍｌ,１０ｍｇ／ｍｌ）,Ｃ组吸入０．１％沙丁胺醇溶液５ｍｌ。观察三组患者吸药后１５ｍｉｎ肺通气功能的变化。结果 吸药后１５ｍｉｎＢ、Ｃ组用力肺活量（ＦＶＣ）、第１ｓ用力呼气容积（ＦＥＶ１）、最在呼气流量（Ｐ     

支气管哮喘患者血浆内皮素1含量及临床意义

采用特异性放射免疫技术测定了２８例支气管哮喘急性发作（发作组）、２２例支气管哮喘临床控制（缓解组）和２０名健康对照者（对照组）的血浆内皮素１（ＥＴ１）含量。结果显示：发作组血浆含量（１３．４±５．２ｐｍｏｌ／Ｌ）分别显著高于缓解组（８．４±３．９ｐｍｏｌ／Ｌ，Ｐ＜０．０１）和对照组（６．６±２．６ｐｍｏｌ／Ｌ，Ｐ＜０．０１）；而缓解组与对照组间的差异无显著性；发作组血浆ＥＴ１含量分别与血氧分压（ＰａＯ＿２）和一秒钟用力呼气容积占用力肺活量比值（ＦＥＶ＿１％）呈显著负相关（ｒ＝－０．８２５７，ｒ＝－０．８１５７，Ｐ＜０．０１）。上述结果提示ＥＴ１可能涉及到支气管哮喘急性发作的病理生理过程。     

稳定期慢性阻塞性肺疾病患者运动性低氧血症的预测

通过稳定期慢性阻塞性肺疾病（ＣＯＰＤ）患者静息肺功能,以预测运动性低氧血症（ＥＩＨ）发生的可能性。对象与方法　选择稳定期ＣＯＰＤ患者３０例,诊断符合１９９７年《慢性阻塞性肺疾病诊治规范（草案）》的诊断标准［１］。男２０例,女１０例,平均年龄（５２±１３）岁,排除支气管哮喘、肺源性心脏病及其他系统疾病。静息状态下测患者肺活量（ＶＣ）为（３－１±０－７）Ｌ,一秒钟用力呼气容积（ＦＥＶ１）为（１－７±１－９）Ｌ,最大通气量（ＭＶＶ）为（６７±３７）Ｌ／ｍｉｎ,肺一氧化碳弥散量占预计值百分比（ＤＬＣＯ％…     

呋塞米吸入治疗对老年慢性哮喘患者肺功能和外周血T淋巴细胞亚群的影响

目的评价呋塞米（速尿）吸入对老年人慢性哮喘的治疗效果。方法７２例老年慢性哮喘患者分别给予速尿（Ａ组）、速尿＋溴化异丙托品（Ｂ组）和溴化异丙托品（Ｃ组）治疗，每组各２４例，并与６０例非老年慢性哮喘患者的结果进行比较。吸入前后测肺功能〔最大肺活量（ＦＶＣ）、一秒钟最大呼气量（ＦＥＶ１）、最大呼气流速（ＰＥＦＲ）〕和外周血Ｔ细胞亚群。结果老年组总有效率（有效＋显效），Ａ、Ｂ、Ｃ组分别为７５％、９２％、６７％。肺功能和Ｔ细胞亚群改变：Ａ组ＦＥＶ１和ＣＤ４吸入前后变化差异有显著性（Ｐ＜００５）；Ｂ组肺功能指标和ＣＤ４、ＣＤ８、ＣＤ４／ＣＤ８差异有非常显著性（Ｐ＜００１或０００１）；Ｃ组除ＰＥＦＲ有显著变化（Ｐ＜００５）外，余项也有改善，但无统计学意义。非老年组的疗效与老年组疗效基本相同。结论速尿吸入对老年人慢性哮喘有防治作用，特别是速尿＋溴化异丙托品联合吸入效果更好     

Bronchial hyperresponsiveness and exhaled nitric oxide in patients with cardiac disease

BACKGROUND: Increased concentrations of exhaled nitric oxide (NO) correlate with increased airway inflammation and measurement of exhaled NO is a noninvasive method for the management of bronchial asthma. In various cardiac diseases, bronchial hyperresponsiveness is observed, as is bronchial asthma. However, there have been few studies on the relationship between exhaled NO and bronchial responsiveness in cardiac diseases. OBJECTIVE: The aim of this study was to clarify the association between exhaled NO and bronchial hyperresponsiveness in patients with cardiac disease. METHODS: We measured expired NO and bronchial responsiveness to inhaled methacholine in 19 patients with cardiac diseases and 17 with bronchial asthma. We divided the cardiac disease patients into two groups according to their bronchial responsiveness to inhaled methacholine: BHR(+) group consisted of 12 patients with bronchial hyperresponsiveness and BHR(-) group consisted of 7 patients without bronchial hyperresponsiveness. RESULTS: The concentration of exhaled NO in the asthmatic patients was significantly higher than that in the BHR(+) and BHR(-) groups (142.0 +/- 17.0, 33.6 +/- 6.4 and 42.3 +/- 10.3 ppb, respectively, p < 0.01). There was no significant difference in exhaled NO between BHR(+) and BHR(-) groups. There were also no significant differences in the parameters of bronchial hyperresponsiveness between the cardiac BHR(+) and bronchial asthma groups. These results indicate that bronchial hyperresponsiveness in patients with cardiac diseases is not a consequence of eosinophilic inflammation or of exhaled NO. CONCLUSION: We conclude that bronchial hyperresponsiveness in patients with cardiac diseases can occur independently of NO production.     

Inhaled fluticasone decreases bronchial but not alveolar nitric oxide output in asthma.

Exhaled nitric oxide (NO) concentration is a noninvasive measure of airway inflammation and is increased in asthma. Inhaled glucocorticoids decrease exhaled NO concentration, but the relative contributions of alveolar and bronchial levels to the decrease in exhaled NO concentration are unknown. Alveolar NO concentration and bronchial NO flux can be separately approximated by measuring exhaled NO at several exhalation flow rates. The effect of steroid treatment on alveolar and bronchial NO output in asthma was studied. Alveolar NO concentration and bronchial NO flux were assessed in 16 patients with asthma before and during treatment with inhaled fluticasone for 8 weeks and in 16 healthy controls. Before the treatment, asthmatics had increased bronchial NO flux (mean+/-SEM: 3.6+/-0.4 versus 0.7+/-0.1 nL x s(-1), p<0.001) but normal alveolar NO concentration (1.2+/-0.5 versus 1.0+/-0.2 parts per billion (ppb), p>0.05) compared with controls. Inhaled fluticasone decreased bronchial NO flux from 3.6+/-0.4 to 0.7+/-0.1 nL x s(-1) (p<0.01) but had no effect on alveolar NO concentration (before: 1.2+/-0.5; after: 1.2+/-0.1 ppb, p>0.05). The forced expiratory volume in one second improved, whereas asthma symptom score and serum levels of eosinophil cationic protein and eosinophil protein X decreased during the treatment. In conclusion, inhaled fluticasone decreases bronchial but not alveolar nitric oxide output simultaneously with clinical improvement in patients with asthma.     

Effects of inducible nitric oxide synthase inhibition in bronchial vascular remodeling-induced by chronic allergic pulmonary inflammation

Vascular remodeling is an important feature in asthma pathophysiology. Although investigations suggested that nitric oxide (NO) is involved in lung remodeling, little evidence established the role of inducible NO synthase (iNOS) isoform in bronchial vascular remodeling. The authors investigated if iNOS contribute to bronchial vascular remodeling induced by chronic allergic pulmonary inflammation. Guinea pigs were submitted to ovalbumin exposures with increasing doses (1～5 mg/mL) for 4 weeks. Animals received 1400W (iNOS-specific inhibitor) treatment for 4 days beginning at 7th inhalation. Seventy-two hours after the 7th inhalation, animals were anesthetized, mechanical ventilated, exhaled NO was collected, and lungs were removed and submitted to picrosirius and resorcin-fuchsin stains and to immunohistochemistry for matrix metalloproteinase-9 (MMP-9), tissue inhibitor of metalloproteinase-1 (TIMP-1), and transforming growth factor-β (TGF-β). Collagen and elastic fiber deposition as well as MMP-9, TIMP-1, and TGF-β expression were increase in bronchial vascular wall in ovalbumin-exposed animals. The iNOS inhibition reduced all parameters studied. In this model, iNOS inhibition reduced the bronchial vascular extracellular remodeling, particularly controlling the collagen and elastic fibers deposition in pulmonary vessels. This effect can be associated to a reduction on TGF-β and on metalloproteinase-9/TIMP-1 vascular expression. It reveals new therapeutic strategies and some possible mechanism related to specific iNOS inhibition to control vascular remodeling.     

Prostaglandins and bronchial asthma (author's transl)]

Prostaglandins (PG) show different effects on the bronchomotoric excitability depending on the fact to which group they certain. The best investigated PG are PGE1, PGE2 (bronchodilators) and PGF2a (bronchoconstrictor). It is possible that PG play a certain role in the pathogenesis of bronchial asthma. Among other hypotheses, the influence upon adenylate cyclase - cAMP systems (without affecting the adrenoreceptors) is evident. Probably, PG exert a regulatory function on bronchial tone. The pathogenetic imporatnce of PG metabolites for bronchial asthma is discussed. A therapeutical influence upon bronchial asthma is theoretically possible on four ways: by 1) stimulation of partial endogenous synthesis of PGE, 2) inhibition of the biotransformation of PGE, 3) exogenous application of PGE, i.e. development of PGE derivatives indifferent to bronchial mucosa, stable in solution and relatively resistant to biotransformation and 4) inhibition of biosynthesis of PGF2a. The development of synthetic PGE1 derivatives (15-methyl-11-desoxy-PGE1) appears to be of future importance. Summarizing we can say that, at the present stage of development, a directed therapeutic utilization of PG for bronchial asthma seems to be of low probability yet. The problem of aspirin-induced asthma including all its practical consequences is discussed.     

Gastric Asthma: An Unrecognized Disease with an Unsuspected Frequency

Bronchial asthma is a disease that has been recognized for centuries, which is influenced mainly by genetic and environmental factors. The current interest of bronchial asthma is focused to ascertain the causes and the mechanisms that induce bronchoconstriction. Recently, abnormalities of the esophageal and gastric tracts have become important related areas for research. In predisposed individuals, these abnormalities can trigger or worsen the particular syndrome better known as “gastric asthma.” In bronchial asthma the disorder of gastroesophageal reflux (GER) occurs more often than would be expected by chance. The neurogenic mechanism is considered to be the main cause of bronchoconstriction. The diagnosis of gastric asthma is particularly difficult and it should be considered also when GER is less evident or not recognized. In asthmatic patients the recognition of gastric abnormalities is very relevant for therapeutic problems also when GER is in a subclinical stage. In fact, many drugs used in the treatment of bronchial asthma can promote or enhance GER and subsequently they can worsen the symptoms of gastric asthma.     

Quality of life and inflammatory markers in mild asthma

STUDY OBJECTIVES: The aim of this study was to explore the relationship between quality of life and measures of asthma, such as lung function, reversibility to bronchodilation, exhaled nitric oxide (NO), and bronchial responsiveness to direct and indirect stimulus in patients with mild asthma in a primary care setting.Patients and measurements: Seventy-seven asthmatic patients not treated with glucocorticosteroids completed the Asthma Quality of Life Questionnaire. Spirometry was performed before and after bronchodilation, and bronchial challenges with methacholine and eucapnic dry air hyperventilation were conducted on separate days. NO in exhaled air and serum IgE were also analyzed. RESULTS: We found no correlation between quality of life and any of the other parameters. There was a significant covariation between exhaled NO and bronchial responsiveness to methacholine and dry air, and also between FEV(1) (percentage of predicted) and reversibility to a bronchodilator. The levels of exhaled NO were higher in the asthmatic subjects with atopy than in the nonatopic asthmatics. CONCLUSIONS: The measures used in our study do not reflect health-related quality of life in subjects with mild asthma. We conclude that in the clinical situation, quality of life and other measures of asthma provide complementary information.     

Messung des exhalierten Stickstoffmonoxids (NO) bei Kindern und Jugendlichen

The endogenous trace gas nitric oxide (NO) is involved in the regulation of host defence, ventilation-perfusion matching and ciliary function. Standard procedures, reference data and devices are available to determine its breath concentration. Preschool and school age children will be able to exhale against a resistance for online measurement; mixed air is sampled in younger children. A large amount of paediatric data has been gathered on fractional exhaled NO at a flow of 50?ml/s. This parameter reflects bronchial NO flux and is diagnostically sensitive and specific for allergic asthma. Although its role in monitoring and treatment of asthmatic children remains controversial, a normal result can reliably exclude bronchial hyperreactivity and consecutive loss of symptom control after therapeutic step-down. Nasal nitric oxide can be measured as a screening marker for primary ciliary dyskinesia. This article discusses basic principles and clinical context of exhaled NO measurements and advocates a rational use by paediatric respiratory specialists.     

Childhood asthma: exhaled nitric oxide in relation to clinical symptoms.

Bronchial asthma is associated with increased levels of exhaled nitric oxide which are suppressible by glucocorticosteroid inhalation. Children with bronchial asthma were studied to elucidate the relation between endogenous NO release and recent symptoms of bronchial obstruction. Twenty-five children with atopic asthma and 11 healthy control subjects were enrolled and exhaled NO was studied using chemiluminescence analysis. The subjects breathed purified air (<0.5 parts per billion (ppb) NO) exclusively through their mouths. Orally expired NO was measured during continuous nasal aspiration (1.3 L x min(-1)) to remove nasally produced NO. Nasal NO concentration was determined within the aspirated gas. Orally expired NO concentration was 2.5+/-0.3 ppb (mean +/-SEM) in healthy control subjects, 3.19+/-0.88 ppb (NS) in symptom-free children, and 8.28+/-0.81 ppb (p< or =0.01) in children with bronchial asthma who had had recent symptoms of bronchial obstruction. Similarly, in the subgroup of children treated regularly with inhaled glucocorticosteroids those with recent symptoms had significantly higher orally exhaled NO concentrations than healthy control subjects (9.5+/-1.5 ppb, p<0.05). The nasal NO concentration was 152.8+/-12.7 ppb in healthy control subjects and not significantly different in asthmatic children. In this group of asthmatic children, recent symptoms of bronchial obstruction were linked to significantly higher concentrations of NO in orally exhaled gas and to increased oral NO excretion rates. If substantiated by further studies, measurement of orally exhaled NO during nasal aspiration may become useful to monitor disease control in asthmatic children.     

Exhaled nitric oxide; relationship to clinicophysiological markers of asthma severity

Bronchial asthma is an airway disorder associated with bronchial hyperresponsiveness, variable airflow obstruction and elevated levels of nitric oxide (NO) in exhaled air. The variables all reflect, in part, the underlying airway inflammation in this disease. To understand their interrelationships we have investigated the relationship between exhaled NO levels and clinicophysiological markers of asthma severity. Twenty-six steroid naive atopic asthmatics participated in the analysis. All were given diary cards and were asked to record their peak expiratory flow (PEF) rates twice daily together with their asthma symptom scores and beta-agonist use. Diary cards were collected 2 weeks later and measurements of exhaled NO levels, FEV1 and histamine bronchial hyperreactivity (PC20 histamine) were undertaken. Exhaled NO levels were significantly higher in our study population than in normal control subjects and correlated negatively with PC20 histamine (r = -0.51; P = 0.008) and positively with PEF diurnal variability (r = 0.58; P = 0.002), but not with symptom scores, beta-agonist use of FEV1 (%). We conclude that a significant relationship exists between exhaled NO levels and the two characteristic features and markers of asthma severity, namely bronchial hyperreactivity and PEF diurnal variability. The lack of correlation between symptom score and beta-agonist use, of FEV1 (%) predicted and exhaled NO suggests that these measures are reflective of differing aspects of asthma.     

Extended exhaled NO measurement differentiates between alveolar and bronchial inflammation

Lower respiratory tract inflammation can be detected by measuring exhaled nitric oxide (NO) concentration at a single exhalation flow rate, but this does not differentiate between alveolar and bronchial NO production. We assessed alveolar NO concentration and bronchial NO flux with an extended method of measuring exhaled NO at several exhalation flow rates in 40 patients with asthma, 17 patients with alveolitis, and 57 healthy control subjects. Bronchial NO flux was higher in asthma (2.5 +/- 0.3 nl/s, p < 0.001) than in alveolitis (0.7 +/- 0.1 nl/s) and healthy control subjects (0.7 +/- 0.1 nl/s). Alveolar NO concentration was higher in alveolitis (4.1 +/- 0.3 ppb, p < 0.001) than in asthma (1.1 +/- 0.2 ppb) and healthy control subjects (1.1 +/- 0.1 ppb). In asthma, bronchial NO flux correlated with serum level of eosinophil protein X (EPX) (r = 0.60, p < 0.001) and bronchial hyperresponsiveness (r = 0.55, p < 0.001). In alveolitis, alveolar NO concentration correlated inversely with pulmonary diffusing capacity (r = -0.55, p = 0.022) and pulmonary restriction. Glucocorticoid treatment or allergen avoidance normalized bronchial NO flux in asthma and decreased alveolar NO concentration toward normal in alveolitis. In conclusion, extended exhaled NO measurement can be used to separately assess alveolar and bronchial inflammation and to assess disease activity/severity in asthma and alveolitis.