呼气末正压对不同肺部病变重症患者腹内压的影响

目的 探讨呼气末正压(PEEP)对不同肺部病变重症患者腹内压(IAP)的影响.方法 选择2012年1月至2016年12月本院重症医学科进行机械通气的重症患者72例,按照肺部病变分为慢性阻塞性肺疾病(COPD)组、急性呼吸窘迫综合征(ARDS)组及无胸肺部疾患组各24例,观察患者在平卧位时PEEP分别为0、3、6、9、12和15 cmH2O(1 cmH2O=0.098 kPa)条件下的IAP、肺顺应性(CL)、总顺应性(CT)及胸廓顺应性(CTH)的变化,并分析IAP与PEEP、CL、CT、CTH的关系.结果 PEEP对不同肺部病变重症患者IAP的影响:ARDS组＜无胸肺部疾患组＜COPD组(P＜0.05);各组患者肺顺应性:ARDS组＜无胸肺部疾患组＜ COPD组(P＜0.05).相关分析显示,IAP与PEEP存在明显的线性相关(r=0.92,P＜0.01),IAP与CL、CT、CTH存在明显的线性相关(r=0.83、0.64、-0.56,P均＜0.05).结论 不同肺部病变状态下PEEP对IAP的影响不同,其中COPD患者影响较大,而ARDS患者影响较小;影响的大小与肺顺应性大小一致.     

血浆置换联合连续性静脉-静脉血液滤过对急性呼吸窘迫综合征治疗的临床观察

目的研究血浆置换（PE）联合连续性静脉-静脉血液滤过（CVVH）治疗急性呼吸窘迫综合征（ARDS）的疗效。方法20例急性呼吸窘迫综合征患者除经内科常规治疗外,行PE联合CVVH）,连续测定心率（HR）、平均动脉压（MAP）、中心静脉压（CVP）,pH、动脉血氧分压（PaO2）、动脉血二氧化碳分压（PaCO2）,氧合指数（PaO2/FiO2）、肺动态顺应性（Cdyn）、气道阻力（Raw）,同时抽取静脉血2ml测定血液C反应蛋白（CRP）的浓度。并进行ICU监护的结果记录以APACHEII评分及SIRS评分判断患者病情的变化。结果在治疗过程中,血流动力学稳定,血浆置换前后及CVVH治疗前与治疗后相比HR、MAP、CVP,pH、PaO2、PaCO2,其中脉血PaO2、动脉血FiO2、Cdyn、明显升高,Raw明显下降（P〈0.05）,血浆置换后C反应蛋白（CRP）的浓度明显下降（P〈0.05）,CVVH治疗前与治疗后相比APACHEII评分及SIRS评分差异有统计学意义（P〈0.05）。结论PE联合CVVH治疗可显著改善急性呼吸窘迫综合征患者的临床症状,有效改善急性呼吸窘迫综合征的预后。     

沙丁胺醇对慢性阻塞性肺疾病患者单肺通气早期呼吸力学的影响

目的麻醉诱导前吸入硫酸沙丁胺醇气雾剂(万托林),观察其对单肺通气早期呼吸力学的影响。方法合并慢性肺阻塞疾患(COPD)拟行肺叶切除手术的患者40例,随机分成观察组和对照组各20例,观察组:患者给予万托林200μg(2揿)后面罩吸氧;对照组:单纯面罩吸氧,30 min后开始麻醉诱导。记录监测时点的血气分析以及气道峰压、气道平台压、气道阻力、胸肺顺应性的变化。结果麻醉诱导前、双肺通气、单肺通气10 min及20 min的PaCO2观察组低于对照组,PaO2观察组高于对照组,P<0.05或P<0.01。双肺通气、单肺通气10 min及20 min的气道峰压、气道平台压、气道阻力观察组低于对照组,胸肺顺应性观察组高于对照组,P<0.05。结论硫酸沙丁胺醇气雾剂能降低COPD患者单肺通气早期的气道压力和气道阻力,增加胸肺顺应性,有利于术中呼吸管理,提高了麻醉手术的安全性。     

适应性支持通气在COPD合并呼吸衰竭患者的应用

目的比较适应性支持通气(ASV)和同步间歇指令通气(SIMV)对慢性阻塞性肺疾病(COPD)合并呼吸衰竭患者内源性呼气末正压(PEEPi)和呼吸功的影响。方法 30例有自主呼吸的COPD合并呼吸衰竭患者,在同样的设置下,先予以SIMV模式通气60 min,后改为ASV模式通气60min,结束后再次回到SIMV模式通气60 min。记录上述三个60 min后的呼吸力学等参数。结果 ASV模式下的平台压下降明显(P<0.01);ASV模式PEEPi的发生率较SIMV模式明显下降(P<0.05);器械附加功(WOBimP)和吸气压力时间乘积(PTP)均小于SIMV下的参数(P<0.01)。结论在部分支持通气过程中,ASV相对于SIMV,能明显改善高通气力学状态,有利于降低呼吸负荷和呼吸做功。     

COMPUTER SIMULATIONS OF PARTICLE DEPOSITION IN THE LUNGS OF CHRONIC OBSTRUCTIVE PULMONARY DISEASE PATIENTS

Epidemiology data show that mortality rates for chronic obstructive pulmonary disease (COPD) patients increase with an increase in concentration of ambient particulate matter (PM). This is not seen for normal subjects. Therefore, the U.S. Environmental Protection Agency (EPA) has identified COPD patients as a susceptible subpopulation to be considered in regulatory standards. In the present study, a computer model was used to calculate deposition fractions of PM within the lungs of COPD patients. The morphology of COPD lungs was characterized by two distinct components: obstruction of airways (chronic bronchitis component), and degeneration of alveolar structure (emphysema component). The chronic bronchitis component was modeled by reducing airway diameters using airway resistance measurements in vivo, and the emphysema component was modeled by increasing alveolar volumes. Calculated results were compared with experimental data obtained from COPD patients for controlled breathing trials (tidal volume of 500 ml, respiratory time of 1 s) with a particle size of 1 µm. The model successfully depicts PM deposition patterns and their dependence on the severity of disease. The findings indicate that airway obstructions are the main cause for increased deposition in the COPD lung.     

Effects of Lung Surfactant Factor (LSF) Treatment on Gas Exchange and Histopathological Changes in an Animal Model of Adult Respiratory Distress Syndrome (ARDS): Comparison of Recombinant LSF with Bovine LSF

Summary: Repetitive lung lavage of adult rats leads to lung injury similar to ARDS resulting in poor gas exchange, protein leakage and infiltration of polymorphonuclear neutrophils (PMN) into the alveolar spaces (J Appl Physiol 1983; 55: 131-138). In a previous dose response comparison we have demonstrated that poor gas exchange could be improved by lung surfactant factor (LSF) instillation soon after lavage. Since Surfacten® (Tokyo Tanabe Co. Ltd., Tokyo, Japan) was described in vitro to inhibit PMN activity, we compared this preparation with a Recombinant LSF preparation (Byk Gulden, Konstanz, Germany; phospholipids plus human identical surfactant protein C) at doses of 25, 50 and 100 mg/kg body weight. Their efficacy was compared with an untreated control group with respect to improving gas exchange, inhibition of hyaline membrane formation and inhibition of the inflammatory response after multiple lavage. Tracheotomized rats were pressure-controlled ventilated (Siemens Servo Ventilator 900C, Sweden) with 100% oxygen at a respiratory rate of 30 breaths/min, inspiration:expiration ratio of 1:2, peak inspiratory pressure (PIP) of 28 cmH₂O at positive end-expiratory pressure (PEEP) of 8 cmH₂O. Two hours after LSF administration PEEP was reduced from 8 to 6 cmH₂O (first PEEP-reduction), from 6 to 3 (second reduction) and from 3 to 0 cmH₂O (third reduction) and finally raised to 8 cmH₂O. Results for the averaged partial arterial oxygen pressure [PaO₂ (mmHg)] of the 2 h period [PaO₂(5′-120′)] and for the PaO₂ during the second PEEP reduction [PaO₂(PEEP23/3)] were calculated. Both LSF preparations caused a dose-dependent increase of the PaO₂(5′-120′) and the PaO₂(PEEP23/3). Similarly, the formation of hyaline membranes was inhibited by both LSF preparations in a dose-dependent manner. Inhibition of the inflammatory response (infiltration of PMN) was not effected by either of the LSF preparations at any dose level. The described variations in ventilator settings are useful to evaluate the deflation stability and re-expansion potential of different LSF preparations. The reported results give evidence that prevention of atelectasis by LSF treatment improves gas exchange and inhibits formation of hyaline membranes, leading to the conclusion that LSF treatment may be a promising therapy in ARDS patients.     

Computer simulations of particle deposition in the lungs of chronic obstructive pulmonary disease patients

Epidemiology data show that mortality rates for chronic obstructive pulmonary disease (COPD) patients increase with an increase in concentration of ambient particulate matter (PM). This is not seen for normal subjects. Therefore, the U.S. Environmental Protection Agency (EPA) has identified COPD patients as a susceptible subpopulation to be considered in regulatory standards. In the present study, a computer model was used to calculate deposition fractions of PM within the lungs of COPD patients. The morphology of COPD lungs was characterized by two distinct components: obstruction of airways (chronic bronchitis component), and degeneration of alveolar structure (emphysema component). The chronic bronchitis component was modeled by reducing airway diameters using airway resistance measurements in vivo, and the emphysema component was modeled by increasing alveolar volumes. Calculated results were compared with experimental data obtained from COPD patients for controlled breathing trials (tidal volume of 500 ml, respiratory time of 1 s) with a particle size of 1 microm. The model successfully depicts PM deposition patterns and their dependence on the severity of disease. The findings indicate that airway obstructions are the main cause for increased deposition in the COPD lung.     

SIMV＋AutoFlow对COPDⅡ型呼吸衰竭患者呼吸力学的影响

目的观察慢性阻塞性肺疾病（COPD）Ⅱ型呼吸衰竭患者应用同步间歇指令通气辅用自动变流（SIMV＋AutoFlow）模式时气道峰压（PIP）、平均压（Pmean）、阻力（R）、顺应性（C）和镇静剂使用量,评价SIMV＋AutoFlow对呼吸力学的影响。方法选择需机械通气的COPDⅡ型呼衰患者59例,随机分为2组：Ⅰ组29例选用SIMV＋AutoFlow模式,Ⅱ组30例选用SIMV模式,观察2种模式下患者PIP、Pmean、R、C和镇静剂使用量。结果Ⅰ组在上机后2、24、48h的PIP、Pmean、R及上机72h镇静剂的使用量显著低于Ⅱ组（P〈0.05）;C显著高于Ⅱ组（P〈0.05）;2组患者一般情况、上机前后的血气指标和APACHEⅡ评分差异无统计学意义（P〉0.05）。结论 COPDⅡ型呼吸衰竭患者应用SIMV＋AutoFlow通气模式,能显著降低PIP、Pmean、R,改善呼吸力学,在需要保证输送潮气量,又尽量减少机械通气并发症时,采用SIMV＋AutoFlow是一种较好的方法 。     

Effect of YM-40461, a novel surfactant secretagogue, on chronic obstructive pulmonary diseases and similar symptoms in guinea pigs

YM-40461 (1-(2-dimethylaminoethyl)-1-(3,4,5-trimethoxyphenyl)urea, CAS 142912-85-4), is a novel surfactant secretagogue. The effect of YM-40461 on symptoms, e.g. change of airway functions and hypoxemia, were examined using guinea pigs with induced subacute bronchitis. Bronchitic guinea pigs exhibited basal lung resistance (RL) was 0.152 +/- 0.005 cm H2O/ml/s (normal: 0.130 +/- 0.002 cm H2O/ml/s) and basal lung compliance (CL) of 0.455 +/- 0.011 ml/cm H2O (normal: 0.509 +/- 0.009 ml/cm H2O). Although YM-40461 slightly improved the lung resistance in these animals, it improved significantly and dose-dependently the lung compliance (0.468 +/- 0.008 ml/cm H2O for 1 mg/kg, 0.477 +/- 0.008 for 3 mg/kg, 0.490 +/- 0.011 for 10 mg/kg, p < 0.05 at 10 mg/kg) compared to nontreated bronchitic guinea pigs. YM-40461 improved airway functions in bronchitic guinea pigs just as wall as the beta 2-adrenoceptor agonist salbutamol. Additionally, YM-40461 significantly reduced airway hyperreactivity in response to intravenously infused acetylcholine (ACh). Basal PaO2 was 83.1 +/- 0.7 cm H2O in healthy guinea pigs and 71.2 +/- 1.7 cm H2O in bronchitic guinea pigs, indicating hypoxemia. A dose of 10 mg/kg of YM-40461 relieved hypoxemia in these animals with the values returning to 81.8 +/- 1.9 cm H2O (p < 0.05). These results suggest that YM-40461 ameliorates chronic obstructive pulmonary disease (COPD)-like symptoms in bronchitis models due to increased surfactant in the airway.     

沙丁胺醇联合呼气末正压通气对COPD患者生理功能的影响

目的：观察沙丁胺醇联合外源性呼气末正压通气（PEEPe）对慢性阻塞性肺疾病（COPD）患者生理功能的影响。方法：将对支气管扩张剂有反应性,伴有中度内源性呼气末正压通气（PEEPi）的机械性通气COPD患者10例,分别在插管后30min（ZEEPe-1）,雾化吸入5mg沙丁胺醇后30min（ZEEPe—S）,首次雾化吸入沙丁胺醇后8h到PEEPe通气前的15min（ZEEPe-II）,在基础水平PEEPi上设置PEEPe后30min（PEEPe-30）,雾化吸入5mg沙丁胺醇和PEEPe结合治疗后30min（PEEPe-S）时,评测患者的呼吸系统力学、血液动力学和气体交换功能。在PEEPe通气前检测确定变量的基础值。结果：与ZEEPe-1时间点比较,ZEEPe-S时间点最大总呼气阻力、最小呼吸阻力、附加肺呼吸阻力、功能残气量的变化、PEEPi、肺毛细血管楔压和全身血管阻力均显著降低（P〈0．01）,心率、混合静脉血氧饱和度和氧输送量显著提高（P〈0．01）;在PEEPe-30治疗时间点PEEPi、二氧化碳分压和静脉血掺杂比显著降低（P〈0．01）;在PEEPe-S时间点最大总呼气阻力、最小呼吸阻力、功能残气量的变化、肺毛细血管楔压、静脉血掺杂比和全身血管阻力显著降低（P〈0．01）,心率、氧输送量和动脉血氧分压显著提高（P〈0．01）。结论：对于有中度PEEPi-COPD患者,沙丁胺醇联合PEEPe有累加的治疗作用。     

Reactive nitrogen species in the respiratory tract

Endogenous Nitric Oxide (NO) plays a key role in the physiological regulation of airway functions. In response to various stimuli activated inflammatory cells (e.g., eosinophils and neutrophils) generate oxidants ("oxidative stress") which in conjunction with exaggerated enzymatic release of NO and augmented NO metabolites produce the formation of strong oxidizing reactive nitrogen species, such as peroxynitrite, in various airway diseases including asthma, chronic obstructive pulmonary diseases (COPD), cystic fibrosis and acute respiratory distress syndrome (ARDS). Reactive nitrogen species provoke amplification of inflammatory processes in the airways and lung parenchyma causing DNA damage, inhibition of mitochondrial respiration, protein dysfunction and cell damage ("nitrosative stress"). These effects alter respiratory homeostasis (such as bronchomotor tone and pulmonary surfactant activity) and the long-term persistence of "nitrosative stress" may contribute to the progressive deterioration of pulmonary functions leading to respiratory failure. Recent studies showing that protein nitration can be dynamic and reversible ("denitration mechanisms") open new horizons in the treatment of chronic respiratory diseases affected by the deleterious actions of "nitrosative stress".     

Bronchodilator effect of sublingual isosorbide dinitrate in asthma

Summary The bronchodilating effect of 5 mg sublingual isosorbide dinitrate (ISDN) was studied in 10 patients with bronchial asthma, using the doubleblind randomised cross-over method with matched placebo. In a further 20 asthmatics the effect of sublingual ISDN was compared with that of metaproterenol given by a metered dose inhaler to a total dose of 2.25 mg, again using the cross-over method. The forced oscillation method was used to measure respiratory resistance (Rrs) and spirometry was used to measure vital capacity (VC) and forced expiratory volume in one second (FEV₁). 5 minutes after administration of ISDN Rrs had decreased (p<0.05) and VC (p<0.01) and FEV₁ (p<0.01) were significantly increased. The changes were still present after 15, 30 and 60 min. The placebo had no significant effect. ISDN increased FEV₁ less than metaproterenol, and the difference between them was statistically significant (p<0.05). However, there was no significant difference between ISDN and metaproterenol in the improvement in Rrs and VC. Of the total of 30 patients, 11 experienced headache and 4 had transient hypotension after ISDN administration. These side effects subsided spontaneously. It was concluded that sublingual ISDN had a bronchodilating effect in stable asthmatics.     

Muscarinic effect of atrial natriuretic peptide on rabbit airways.

1. The aim of the present work was to investigate under which circumstances atrial natriuretic peptide (ANP) modulates airway resistance. 2. Of the six groups of rabbits (n = 5) studied, three received an infusion of ANP (80 ng min-1 kg-1 i.v.) for a period of 100 min, while the other three were infused with the vehicle. Before receiving the infusion of ANP or the vehicle, the animals were pretreated with atropine (0.5 mg kg-1 i.v.), propranolol (2 mg kg-1 i.v.) or not pretreated. After 75 min of infusion of ANP, bronchoconstriction was induced by inhalation of histamine. Respiratory resistance (Rrs) was measured before and 3, 5, 10, 15 and 20 min post-histamine challenge. 3. Following 75 min of ANP infusion, plasma ANP concentration increased from 153 +/- 52 (mean +/- s.e.mean) to 1441 +/- 203 pg ml-1 (P < 0.05) without affecting baseline Rrs. Control Rrs values (12.5-20.4 cmH2O l-1 s) were significantly increased following the inhalation of histamine (P < 0.001). By themselves, atropine, propranolol or ANP did not modify the histamine-induced increase in Rrs. However, when the animals were pretreated with atropine, ANP infusion significantly reduced the increase in Rrs induced by histamine (30 +/- 2 vs 51 +/- 6 cmH2O l-1 s; P < 0.05). 4. These data suggest that ANP has an indirect modulating effect on the airway smooth muscle and will decrease Rrs when muscarinic receptors are blocked.     

双水平气道正压通气呼吸机治疗慢性阻塞性肺疾病合并呼吸衰竭

目的 评价双水平气道正压通气（BiPAP）呼吸机治疗慢性阻塞性肺疾病（COPD）合并呼吸衰竭的临床价值.方法 比较76例COPD合并呼吸衰竭患者随机经常规治疗（对照组30例）和加用BiPAP呼吸机治疗（治疗组46例）的临床疗效、血气分析的变化及对心率、呼吸频率的影响.结果 治疗组符合临床好转标准42例,对照组19例,两组比较差异有显著意义（P＜0.005）;两组治疗后4、24 h PaO2、PaCO2、呼吸频率及心率的变化比较差异有显著意义（P＜0.001）,并且BiPAP呼吸机组鼻面罩患者依从性较好.结论 正确应用BiPAP呼吸机治疗COPD合并呼吸衰竭能更快地改善患者的通气功能、纠正二氧化碳潴留和低氧血症.     

Alcoholic lung injury: Metabolic,biochemical and immunological aspects

Chronic alcohol abuse is a systemic disorder and a risk factor for acute respiratory distress syndrome (ARDS) and chronic obstructive pulmonary disease (COPD). A significant amount of ingested alcohol reaches airway passages in the lungs and can be metabolized via oxidative and non-oxidative pathways. About 90% of the ingested alcohol is metabolized via hepatic alcohol dehydrogenase (ADH)-catalyzed oxidative pathway. Alcohol can also be metabolized by cytochrome P450 2E1 (CYP2E1), particularly during chronic alcohol abuse. Both the oxidative pathways, however, are associated with oxidative stress due to the formation of acetaldehyde and/or reactive oxygen species (ROS). Alcohol ingestion is also known to cause endoplasmic reticulum (ER) stress, which can be mediated by oxidative and/or non-oxidative metabolites of ethanol. An acute as well as chronic alcohol ingestions impair protective antioxidants, oxidize reduced glutathione (GSH, cellular antioxidant against ROS and oxidative stress), and suppress innate and adaptive immunity in the lungs. Oxidative stress and suppressed immunity in the lungs of chronic alcohol abusers collectively are considered to be major risk factors for infection and development of pneumonia, and such diseases as ARDS and COPD. Prior human and experimental studies attempted to identify common mechanisms by which alcohol abuse directly causes toxicity to alveolar epithelium and respiratory tract, particularly lungs. In this review, the metabolic basis of lung injury, oxidative and ER stress and immunosuppression in experimental models and alcoholic patients, as well as potential immunomodulatory therapeutic strategies for improving host defenses against alcohol-induced pulmonary infections are discussed.     

慢性阻塞性肺病与重叠综合征患者肺功能的比较

摘要 目的 比较单纯慢性阻塞性肺病(慢阻肺)与重叠综合征（overlap syndrome,OS）患者的肺通气功能与气道阻力。方法 纳入2012年10月~2014年8月就诊于天津医科大学总医院呼吸科患者194例,均经询问病史、日间肺功能检查及夜间多导睡眠（Polysomnography, PSG）监测,根据PSG及肺功能检查结果将其分为OS组78例,慢阻肺组76例,健康对照组40例。分别比较3组受试者肺通气功能指标以及脉冲振荡肺功能指标。结果 肺通气功能指标中,OS组与慢阻肺组比较呼气峰流速（peak expiratory flow,PEF）、剩余75%用力肺活量时呼气流速（maximal expiratory flow after 75% of the FVC has not been exhaled,MEF75）显著降低。其中OS（AHI≥30次/h）患者与慢阻肺组比较,除了PEF、MEF75显著降低之外,剩余25%用力肺活量时呼气流速（maximal expiratory flow after 25% of the FVC has not been exhaled,MEF25）、最大呼气中期流量（maximal mid-expiratory flow,MMEF）也明显降低。脉冲振荡肺功能指标中,OS组与慢阻肺组比较,呼吸总阻抗（Zrs）、振荡频率为5HZ时的黏性阻力（R5）、振荡频率为20HZ时的黏性阻力（R20）、共振频率（Fres）显著增加, OS（AHI≥30次/h）患者较慢阻肺组除了Zrs、R5、R20、Fres显著增加外,R5与R20的差值（R5-R20）、振荡频率为5HZ时的弹性阻力（X5）也有显著差异。结论 OS比慢阻肺患者气道阻塞严重,且重度睡眠呼吸紊乱可以加重慢阻肺患者的小气道阻塞。     

双水平气道正压无创通气治疗慢性阻塞性肺疾病合并呼吸衰竭临床研究

目的 探讨双水平气道正压无创通气（BiPAP）对慢性阻塞性肺疾病（COPD）Ⅱ型呼吸衰竭的治疗效果. 方法 42例COPDⅡ型呼吸衰竭患者随机分成治疗组（22例）和对照组（20例）,对照组给予常规抗感染、平喘、祛痰和低浓度氧疗,治疗组除了常规治疗外,加无创机械通气（BiPAP）治疗,观察治疗前后动脉血气中pH、动脉血氧分压（PaO2）、动脉血二氧化碳分压（PaCO2）的变化. 结果 治疗后治疗组和对照组pH、PaO2均升高,PaCO2下降[治疗组分别为（7.38±0.10）、（94.1±4.9）mm Hg（1 mm Hg=0.133 kPa）、（42.7±4.3）mm Hg,对照组分别为（7.36±0.11）、（69.7±3.6）mm Hg、（69.1±3.8）mm Hg],与治疗前相比,差异有统计学意义（P＜0.05）;但治疗组治疗前后PaO2升高与PaCO2下降的差值均高于对照组,差异有统计学意义（P＜0.01）. 结论 BiPAP通气可作为COPD并呼吸衰竭的一线治疗手段.     

慢性阻塞性肺病急性期致病菌及药物敏感分析

目的 探讨慢性阻塞性肺病急性感染期致病菌变化及其耐药性,为合理应用抗生素提供可靠依据。方法 对46例慢性阻塞性肺病急性感染期患者与30例急性下呼吸道感染进行痰菌培养及药物敏感的对照分析。结果 慢性阻塞性肺病急性感染期多为混合菌感染,革兰氏阳性球菌感染减少,革兰氏阴性杆菌、真菌、厌氧菌增多,且耐药性严重,与对照组比较有显著意义。结论 监测慢性阻塞性肺病急性感染期致病菌变化及其耐药性,可指导临床选择抗生素,预测病情进展。     

COPD合并Ⅱ型呼吸衰竭使用BiPAP呼吸机治疗体会

目的通过对41例使用BiPAP无创正压通气的COPD合并Ⅱ型呼吸衰竭患者的病例分析，提高应用BiPAP呼吸机的治疗水平。方法通过对41例COPD合并Ⅱ型呼吸衰竭患者使用呼吸机治疗过程进行分析，总结影响治疗效果的因素。结论在BiPAP呼吸机的使用中适当的心理干预，合理的参数调节配合良好的气道管理，营养支持对COPD合并Ⅱ型呼吸衰竭患者缺氧，二氧化碳潴留的纠正及生活质量的改善起到重要作用。     

Reduced glucocorticoid receptor expression and function in airway neutrophils

Chronic Obstructive Pulmonary Disease (COPD) is a glucocorticoid resistant condition characterised by airway neutrophilia. Reduced glucocorticoid receptor (GR) expression in COPD airway neutrophils may be a mechanism that contributes to glucocorticoid resistance. Our objective was to investigate the expression and function of GR within COPD airway neutrophils. Dual-label immunofluorescence was used to analyse airway neutrophil expression of GR within peripheral lung tissue samples (11 COPD patients, 7 healthy non-smokers [NS]) and induced sputum (7 COPD patients, 7 NS). TNFα and CXCL8 release were measured in neutrophils isolated from induced sputum and peripheral blood (7 COPD patients) in the presence of dexamethasone. In lung tissue, GR was abundantly expressed in macrophages and lymphocytes, but very low expression was observed in neutrophils (means 6.8% and 4.3% in COPD patients and NS respectively). Similarly low expression was observed in sputum neutrophils (means 3.8% and 6.9% in COPD patients and NS respectively). In contrast, GR was expressed by 100% of blood neutrophils. Dexamethasone had less suppressive effect on TNFα and CXCL8 production in vitro by neutrophils from induced sputum compared to neutrophils from paired blood samples. Airway neutrophils have low expression of GR in both COPD patients and controls. The effects of glucocorticoids on cytokine production from airway neutrophils are reduced. Increased numbers of airway neutrophils lacking GR may contribute to glucocorticoid resistance in COPD patients.