气道高反应性患者肺功能特点分析

目的探讨气道高反应患者肺功能特点。方法 220例慢性咳嗽或胸闷患者按支气管激发试验（BPT）结果分阳性组118例,阴性组102例,比较肺功能指标在吸入生理盐水前后的差异。结果阳性组FEV1、FEV1/FVC、FEF 25%、FEF50%、FEF 75%、MMEF较阴性组明显降低（P〈0.01）,吸入生理盐水后阳性组FVC、FEV1、FEF50%及MMEF较阴性组有明显下降（P〈0.05）。Logistic回归显示小气道病变及吸入生理盐水后的△FEV1是BPT阳性结果的危险因素。结论气道高反应患者具有大小气道功能异常特点。小气道病变及吸入生理盐水后FEV1下降率高的患者更易有BPT阳性结果。     

小气道功能与气道高反应性的相关性分析

目的：分析小气道功能与气道高反应的相关性。方法选取2012年10月至2013年5月于北京友谊医院及北京房山区良乡医院呼吸科门诊就诊的符合纳入及排除标准的临床怀疑哮喘的患者110例,用肺通气功能进行支气管激发试验(BPT),比较 BPT 阳性组与阴性组肺通气肺功能参数及小气道异常率,使用受试者工作特征曲线(ROC 曲线)评估 FEF25/FVC、FEF50/FVC、FEF75/FVC、MMEF/FVC 在 BPT 前后的变化量(△FEF25/FVC、△FEF50/FVC、△FEF75/FVC、△MMEF/FVC)对气道高反应的诊断准确性、敏感度及特异度,对阳性组 PD20-FEV1累积量与△FEF25/FVC、△FEF50/FVC、△FEF75/FVC、△MMEF/FVC进行相关性分析。结果 BPT 前后阳性组 FEV1、FEV1/FVC、FEF25、FEF50、FEF75、MMEF、FEF25/FVC、FEF50/FVC、FEF75/FVC、MMEF/FVC与阴性组比较,差异均有统计学意义(P <0.05)。BPT 前后阳性组小气道异常率与阴性组相比,差异均有统计学意义(χ2=22.482,P =0.000;χ2=25.852,P =0.000)。△FEF25/FVC的曲线下面积(AUC)为0.792[95%CI (0.703~0.881)](P =0.000),△FEF50/FVC的 AUC 为0.767[95%CI (0.677~0.858)](P =0.000),△MMEF/FVC 的 AUC 为0.667[95%CI (0.563~0.771)](P =0.004)。△FEF50/FVC、△MMEF/FVC 与 PD20-FEV1呈正相关(r=0.360,P=0.007;r=0.271,P=0.035)。结论存在气道高反应的患者大小气道功能均明显低于气道反应性正常的患者,存在小气道功能异常的患者BPT可能更易出现阳性结果,小气道功能在激发试验前后的变化可以反映气道高反应性的严重程度。     

哮喘患者小气道功能与气道高反应性的关系探讨

目的探讨哮喘患者小气道功能与气道高反应性的关系。方法选取可疑哮喘患者164例进行肺通气功能测定及支气管激发试验(BPT),依据激发试验结果分为AHR阴性组(n=34)、轻度组(n=53)、中度组(n=43)及重度组(n=34),收集临床资料,检测FVC%pred、FEV_1%pred、FEV_1/FVC、PEF%pred、FEF25%pred、FEF50%pred、FEF75%pred、FEF25-75%pred水平,分析患者基础小气道功能与气道高反应性之间的相关性,利用受试者工作特征(ROC)曲线分析小气道功能指标在预测气道反应性中的价值。结果 (1)基础FVC%pred、FEV_1%pred、FEV_1/FVC、PEF%pred、FEF25%pred、FEF50%pred、FEF75%pred、FEF25-75%pred从AHR阴性组、轻度组、中度组到重度组,数值依次递减,差异均有统计学意义(P0.05)。(2)小气道功能障碍的发生率从AHR阴性组、轻度组、中度组到重度组依次递增,差异有统计学意义(P0.001)。(3)以基础FEF25%pred、FEF50%pred、FEF75%pred、FEF25-75%pred作ROC曲线,曲线下面积(AUC)分别为0.80、0.873、0.833、0.879,均大于0.5,差异有统计学意义(P0.001)。结论哮喘患者基础小气道功能指标与气道高反应性密切相关,且对气道反应程度较低或无反应状态的患者有一定的预测价值。     

支气管舒张试验对AECOPD小气道功能影响

目的 探讨支气管舒张试验对慢性阻塞性肺疾病急性加重期(AECOPD)小气道功能影响.方法 分析我院2008年1月至2011年4月38例AECOPD患者,行支气管舒张试验,FEV1、FEF 50％、FEF 75％、MMEF 75/25％行配对t检验.结果 支气管舒张试验在AECOPD及支气管舒张试验阳性组小气道功能均存在显著差异;在支气管舒张试验阴性组,FEV1、FEF 50％存在显著差异,但FEF 75％、MMEF 75/25％无差异.结论 支气管舒张试验可改善AECOPD患者小气道功能,但在支气管舒张试验阴性组小气道功能指标FEF 75％、MMEF 75/25％无改善.     

慢性咳嗽患者小气道病变及气道高反应性对哮喘的预测价值

目的探讨慢性咳嗽患者小气道病变与气道高反应性的相关性及其对早期哮喘的预测价值。方法对广东省中医院呼吸科2004年9月至2006年9月就诊的249例慢性咳嗽患者,用肺功能检测判断有无小气道病变,用支气管激发试验检测其气道反应性;进一步分析小气道病变与气道高反应性之间的相关性及与患者年龄之间的关系。结果249例慢性咳嗽患者中91例有小气道病变,103例患者支气管激发试验阳性;有小气道病变患者的支气管激发试验阳性率(73.63%,67/91)较无小气道病变患者(22.78%,36/158)明显增高,差异有显著性意义(P<0.01)。小气道病变患者中,<40岁组的激发试验阳性率(90.0%,27/30)明显高于≥40岁组(65.57%,40/61),差异有显著性意义(P<0.05)。结论小气道病变是气道高反应性患者的重要特征,可以用来发现早期年轻哮喘患者。     

小气道阻塞与非吸烟女性早期肺腺癌相关性研究

目的探讨小气道阻塞与非吸烟女性早期肺腺癌的关系以及环境暴露与小气道阻塞的相关性。方法采用病例-对照研究方法,纳入非吸烟女性肺腺癌患者85人和对照组85人;用肺功能指标评价小气道情况。结果肺癌组FEF50%、FEF75%、MMEF75/25均较对照组明显下降,差异具有统计学意义(P0.01);有被动吸烟的肺癌患者小气道阻塞调整危险度上升到3.55(95%CI为1.33～9.02),厨房油烟暴露使小气道阻塞的调整危险度由1.90(95%CI为0.84～4.03)上升到3.61(95%CI为1.78～9.13)。结论小气道阻塞与非吸烟女性早期肺腺癌相关;被动吸烟和厨房油烟暴露可能是小气道阻塞的危险因素。     

哮喘儿童肺通气功能检测的临床分析

目的：通过监测哮喘儿童急性发作期与缓解期肺通气功能各指标变化情况,了解其在儿童哮喘病情评估及指导治疗中的作用。方法应用德国Jaeger Master Screen肺功能仪对43例5～12岁哮喘急性发作期和经治疗后进入缓解期的哮喘儿童进行肺通气功能检测,包括大气道指标（ FVC、FEVl、FEV1/FVC、PEF）及小气道指标（ FEF25、FEF50、FEF75、MMEF75/25）,同时收集哮喘患儿病史资料和治疗情况。结果哮喘急性发作期患儿肺功能指标FVC、FEV1、FEV1/FVC、PEF与缓解期及健康对照组儿童比较,差异有统计学意义（ P＜0.01）;哮喘缓解期患儿的FVC、FEV1、PEF与健康对照组比较,差异无统计学意义（ P＞0.05）。小气道功能指标FEF25、FEF50、FEF75、MMEF75/25在哮喘急性发作期患儿中均明显降低,与缓解期组及健康对照组儿童相比差异有统计学意义（ P＜0.01）;哮喘治疗缓解期组中FEF25、FEF50、FEF75、MMEF75/25仍低于健康对照组,差异有统计学意义（ P＜0.05）。哮喘急性发作期不同严重程度患儿的肺通气功能指标（ FVC％pred、FEV1％pred、PEF％pred、FEF25％pred、FEF50％pred、FEF75％pred、MMEF75/25％pred ）随哮喘严重程度增加各指标越低,差异有统计学意义（ P＜0.05）。结论哮喘急性发作期肺通气功能受损,治疗缓解后小气道肺功能指标仍低于正常。肺通气功能的小气道功能指标在儿童哮喘的病情评估及治疗监测指导中意义更大。     

缓解期哮喘患儿的小气道功能和气道高反应性的相关性研究

目的测定缓解期哮喘患儿的气道高反应性和小气道功能,探讨气道高反应性与小气道功能及临床缓解时间的相关性。方法选取我院收治的64例缓解期哮喘患儿进行肺功能测定和支气管激发试验(以乙酰胆碱作为激发剂),以第一秒最大呼气量(FEV1)下降≥20%作为阳性诊断标准,比较乙酰胆碱激发试验(MCC)阳性组和阴性组患儿的小气道各项指标的基础值及下降百分率;以患儿临床缓解时间≤12个月和12个月的时间为依据,比较两组患儿的MCC的阳性率。结果 (1)MCC阳性患者的小气道指标MEF75占预计值、MEF50占预计值以及MEF25占预计值占均显著低于MCC阴性组(P0.05);(2)MCC阳性组比阴性组各项小气道指标(MEF25、MEF50、MEF75)下降的程度大且速度快(P0.05);(3)缓解时间12个月和≤12个月的患儿间支气管激发试验阳性率差异无显著意义(P0.05);(4)FEV1下降百分率与MEF25下降百分率无显著相关(r=0.435,P=0.125),其余小气道指标与FEV1相关系数均约为0.7(P0.01)。结论缓解期哮喘患儿依然存在气道炎症,症状缓解时间12个月的患儿与≤12个月的患儿MCC发生率比较无显著差异。小气道各项指标的基础值及激发试验中、下降百分率与患儿气道高反应性有显著的相关性,具有重要的临床参考价值。     

小气道指标下降率在儿童运动激发试验中的应用

目的探讨小气道指标下降率对儿童运动激发试验结果的预测价值。方法回顾性分析在我院就诊的哮喘及疑诊哮喘患儿共60例,分析患儿小气道指标下降率与FEV₁下降率的相关性,使用受试者工作特征(ROC)曲线评估小气道指标下降率与运动激发试验结果的关系。结果运动激发试验阳性组小气道指标FEF₅₀、FEF₇₅、MMEF下降率均明显高于阴性组,差异有显著统计学意义(P均<0.001)。FEF₅₀、FEF₇₅、MMEF下降率与FEV₁下降率呈正相关(r=0.640、0.657、0.740,P均<0.001)。FEF₅₀、FEF₇₅、MMEF下降率评判运动激发试验阳性的曲线下面积分别为0.926、0.955、0.985(P均<0.001),最佳截断值分别为21.00%(灵敏度和特异度分别为0.818和0.878),29.50%(灵敏度和特异度分别为0.818和1.000),17.50%(灵敏度和特异度分别为0.909和0.980)。结论运动激发试验阳性患儿小气道指标下降率显著升高,小气道指标下降率与FEV₁下降率呈正相关,并对预测运动激发试验结果具有一定参考意义。     

FeNO联合小气道功能指标对哮喘患者气道高反应性的诊断效能分析

［摘要］　目的　分析呼出气一氧化氮(FeNO)联合小气道功能指标对哮喘患者气道高反应性（AHR）的诊断效能。方法　选择2019年9月至2022年3月解放军总医院第一医学中心呼吸与危重症科收治的哮喘初诊患者60例。其中支气管舒张试验(BDT)阳性患者30例（BDT阳性组）;BDT阴性,而支气管激发试验（BPT）阳性患者30例（BPT阳性组）。另选取同时期有哮喘相关症状,但BDT及BPT均为阴性的非哮喘者30例（对照组）。比较三组的一般临床资料,以及FeNO、第1秒用力呼气容积占预计值百分比(FEV₁%pred)、第1秒用力呼气容积占用力肺活量百分比(FEV₁/FVC%)、用力肺活量占预计值百分比(FVC%pred)、用力呼气50%肺活量的瞬间流量占预计值百分比(FEF50%pred)、用力呼气75%肺活量的瞬间流量占预计值百分比(FEF75%pred)、最大呼气中期流量占预计值百分比(MMEF%pred)水平。采用受试者工作特征（ROC）曲线法分析FeNO及小气道功能指标诊断AHR的效能。结果　BDT阳性组和BPT阳性组的FeNO水平显著高于对照组（P<0.05）,但BDT阳性组和BPT阳性组比较差异无统计学意义（P>0.05）。BDT阳性组和BPT阳性组的MMEF%pred、FEF75%pred、FEF50%pred水平低于对照组,小气道功能障碍发生率高于对照组,差异有统计学意义（P<0.05）,但BDT阳性组和BPT阳性组比较差异无统计学意义（P>0.05）。ROC曲线分析结果显示,FeNO、FEF50%pred、FEF75%pred和MMEF%pred均具有诊断AHR的效能（P<0.05）,且FeNO联合小气道功能指标可进一步提高诊断效能,其中以FeNO+FEF50%pred的诊断效能最佳［AUC(95%CI)：0.868（0.780～0.956）］,灵敏度为86.70%,特异度为73.30%。结论　 FeNO联合小气道功能指标能有效诊断哮喘患者AHR,可作为早期轻症哮喘诊断的补充工具。     

Relationship of airway wall thickness to airway sensitivity and airway reactivity in asthma

Airway wall thickening has been assumed to cause airway hyperresponsiveness, but a protective effect against airway narrowing has also been suggested. We investigated the relationship between airway wall thickness as assessed by helical computed tomography and two components of airway responsiveness, airway sensitivity and reactivity, in patients with stable asthma with (n = 23) and without (n = 22) inhaled steroid treatment. A cross-section of the apical bronchus of the right upper lobe was obtained. Airway wall area corrected by body surface area was measured as an index of wall thickness. Airway sensitivity and reactivity were measured by continuous inhalation of methacholine, on the basis of the methacholine respiratory resistance dose-response curve. The eosinophil count in sputum was determined in 16 patients [steroid (+) group] and 14 patients [steroid (-) group]. In both groups of patients, airway sensitivity was not related to airway reactivity. Airway sensitivity was related to eosinophil count [r = 0.57 in the steroid (+) group and r = 0.49 in the steroid (-) group], but not to airway wall thickness. In contrast, airway reactivity negatively correlated with airway wall thickness [r = -0.56 in the steroid (+) group and r = -0.55 in the steroid (-) group] but not with eosinophil count. Our results suggest that airway wall thickening attenuates airway reactivity in patients with asthma. These findings may have important implications in pathophysiology and in the treatment of airway remodeling.     

嗜酸粒细胞性气道炎症与气道高反应性

为了研究气道嗜酸粒细胞聚集和激活对气道反应性的影响，应用多粘菌素Ｂ豚鼠点鼻建立嗜酸粒细胞性气道炎症的动物模型。结果表明，嗜酸粒细胞聚集本身不引起气道高反应性（ＡＨＲ），而已聚集的嗜酸粒细胞激活在ＡＨＲ发生上起重要作用。提示嗜酸粒细胞激活可能是哮喘发作的重要触发因素。     

气道平滑肌支气管哮喘气道重塑研究进展

气道平滑肌在支气管哮喘气道重塑中发生了重要作用.本文就其生物物理学改变,细胞表面离子通道、细胞内钙信号转导的变化,神经调控的特点,以及增殖分泌效应的研究进展作一综述.     

气道神经的可塑性与气道高反应性

多种因素可导致气道神经发生可塑性改变，即支配气道的周围神经、中枢神经在神经递质及其受体、兴奋性和分布密度等方面的改变。气道神经的这些可塑性改变与气道高反应性有密切而复杂的联系，是引起气道高反应性的机制之一。     

The contribution of airway smooth muscle to airway narrowing and airway hyperresponsiveness in disease.

Airway hyperresponsiveness (AHR), the exaggerated response to constrictor agonists in asthmatic subjects, is incompletely understood. Changes in either the quantity or properties of airway smooth muscle (ASM) are possible explanations for AHR. Morphometric analyses demonstrate structural changes in asthmatic airways, including subepithelial fibrosis, gland hyperplasia/hypertrophy, neovascularization and an increase in ASM mass. Mathematical modelling of airway narrowing suggests that, of all the changes in structure, the increase in ASM mass is the most probable cause of AHR. An increase in ASM mass in the large airways is more closely associated with a greater likelihood of dying from asthma than increases in ASM mass in other locations within the airway tree. ASM contraction is opposed by the elastic recoil of the lungs and airways, which appears to limit the degree of bronchoconstriction in vivo. The cyclical nature of tidal breathing applies stresses to the airway wall that enhance the bronchodilating influence of the lung tissues on the contracting ASM, in all probability by disrupting cross-bridges. However, the increase in ASM mass in asthma may overcome the limitation resulting from the impedances to ASM shortening imposed by the lung parenchyma and airway wall tissues. Additionally, ASM with the capacity to shorten rapidly may achieve shorter lengths and cause a greater degree of bronchoconstriction when stimulated to contract than slower ASM. Changes in ASM properties are induced by the process of sensitization and allergen-exposure such as enhancement of phospholipase C activity and inositol phosphate turnover, and increases in myosin light chain kinase activity. Whether changes in ASM mass or biochemical/biomechanical properties form the basis for asthma remains to be determined.     

Clinical relevance of airway remodelling in airway diseases.

Asthma and chronic obstructive pulmonary disease (COPD) are characterised by airflow obstruction, airway remodelling (measurable structural change) and inflammation. The present review will examine the relationship between airway remodelling in these two conditions with respect to symptoms, abnormal lung function, airway hyperresponsiveness and decline in lung function. The potential for remodelling to be a protective response will also be discussed. Asthma is associated with variable symptoms and changes in lung function and also fixed abnormalities of lung function and an increased rate of decline in lung function with age. There is a relative preservation of the relaxed airway lumen dimensions, prominent thickening of the smooth muscle layer and reduced airway distensibility. The severity of asthma is related to the degree of airway remodelling, which is most marked in cases of fatal asthma. In COPD, symptoms are persistent and predictable but also progressive and are related to fixed abnormalities of lung function. Remodelling is associated with narrowing of the airway lumen and an increased thickness of the airway wall, although not usually to the extent seen in asthma. COPD is most often due to smoking where there is also remodelling of the parenchyma that may contribute to symptoms.     

The pharyngeo-tracheal lumen airway: an assessment of airway control in the setting of upper airway hemorrhage

Aspiration of blood from nasal and upper airway injuries is a common problem in trauma patients. The pharyngeo-tracheal lumen (PTL) airway uses a large balloon to occlude the oropharynx. We conducted a postmortem radiographic evaluation of the PTL airway's ability to control simulated upper airway hemorrhage using a barium solution. The PTL airway was inserted in ten patients and the barium solution was instilled in the nose until it was full. Radiographs were taken to determine the extent of containment of the radiopaque liquid. The PTL airway successfully controlled the simulated upper airway hemorrhage in nine of the ten cases studied including one patient with a cleft palate. There was leakage in the tenth case due to a balloon leak. The PTL airway may be the prehospital airway of choice in trauma patients due to its ability to control upper airway hemorrhage, but it requires further clinical testing.     

Baseline airway hyperresponsiveness and its reversible component: role of airway inflammation and airway calibre.

Airway hyperresponsiveness (AHR), in which airway inflammation has been reported to be a key factor, is an important component of asthma. However the precise role of inflammation in AHR is still unclear. In this report, airway inflammatory changes were assessed using hypertonic saline-induced sputum examination and exhaled nitric oxide analysis, and the relation between AHR to methacholine, airway calibre forced expiratory volume in one second (FEV1) and airway inflammatory indices examined. Furthermore, the changes in these variables were also examined by means of 8 weeks' open uncontrolled inhaled steroid administration (800 microg x beclomethasone x day(-1)). Asthmatic subjects had higher eosinophil counts and bradykinin concentration in induced sputum and higher exhaled NO levels, and showed AHR to methacholine. Baseline AHR significantly correlated with FEV1 but not with indices of inflammation in sputum or exhaled air. Steroid inhalation therapy was associated with a reduction in eosinophil and bradykinin concentration in sputum and NO levels in exhaled air and an improvement in FEV1 and AHR. The changes in FEV1 and AHR were significantly related to changes in markers in sputum and exhaled air (p<0.01 for each). These results suggest that baseline airway hyperresponsiveness can be predicted from the airway calibre but not from inflammatory parameters in sputum or exhaled air. In contrast, the reversible component of airway hyperresponsiveness appeared to be associated with the reduction in airway inflammation.     

Organ-cultured airway explants: a new model of airway hyperresponsiveness

Respiratory pathology research is limited by the number of appropriate multicellular models suitable for studying mechanical properties and signaling pathways that are involved in airway responsiveness. In this study, the electrophysiological and pharmacomechanical properties of organ-cultured explants derived from normal guinea pig bronchi and trachea were investigated. The explants maintained their basic histological phenotype but became hyperreactive to excitatory (muscarinic, histaminergic, serotinergic, and thromboxane receptor agonists, 60 mM KCl) and inhibitory (norepinephrine, isoproterenol) stimuli within the first 3 days in culture, with or without serum in the culture medium. Indomethacin pretreatment did not modify the spasmogen responses of the explant. The onset of this intrinsic overreactivity was highly dependent on the initial presence of epithelium, took 3 days to reach its maximum, and lasted over several days (days 3 to 7). Removal of Ca2+ from the bathing solution initially normalized the inotropic responses of the cultured versus freshly isolated airway tissues. However, the responses to repetitive carbachol challenges in the absence of Ca2+ displayed a slower inactivation in the cultured explants compared to fresh tissues. Smooth muscle resting membrane potential and potassium-induced depolarizations were unaffected by organ culture. Immunohistochemical analyses revealed the presence of apoptotic bodies in the submucosa and epithelial layers, but none in the smooth muscle layer of cultured airways. These functional and histological findings may prove useful in understanding signaling processes involved in tissue hyperresponsiveness related to asthma.