Effects of hydralazine on hemodynamics, ventilation, and gas exchange in patients with chronic obstructive pulmonary disease and pulmonary hypertension

Reports on hemodynamic effects of hydralazine on pulmonary hypertension (primary or secondary) usually include cases with severe disease or with mixed varieties of pulmonary vascular disease. Serious side effects and death have been reported. Effects of this drug on ventilation and gas exchange are unknown. We investigated the short-term effects of hydralazine treatment on hemodynamics, ventilation, and gas exchange in a relatively homogeneous group of patients with severe chronic obstructive pulmonary disease and moderate exertional pulmonary hypertension (mean pulmonary artery pressure, 43 +/- 3 mmHg). Hydralazine produced significant improvement in cardiac index, total pulmonary resistance, and oxygen transport. We also observed significant improvement in alveolar ventilation (mean PaCO2, decreased from 47 +/- 2 to 40 +/- 3 mmHg at rest and from 51 +/- 3 to 43 +/- 3 mmHg during exercise). The severe exertional hypoxemia of the group (mean PaO2, 48 +/- 2 mmHg) improved significantly (mean PaO2, 57 +/- 3 mmHg). Four of 11 patients showed increased exercise tolerance after hydralazine. This change is probably related to a combined improvement in hemodynamics plus a newly observed improvement in gas exchange and ventilation. Three of 14 patients could not tolerate hydralazine because of marked tachycardia. Serious side effects were not observed in the remaining group.     

Prognostic value of mouth occlusion pressure in patients with chronic ventilatory failure

BACKGROUND: Mouth occlusion pressure measurement is widely used for assessment of respiratory muscle function, particularly in patients with respiratory failure. However, its predictive value for long-term survival remains largely unexplored. METHODS: In 464 patients with chronic hypercapnic respiratory failure (CHRF) due to various underlying disorders and receiving non-invasive ventilation (NIV), maximal inspiratory mouth pressure (PI(max)), mouth occlusion pressure at 100 ms during quiet breathing (P(0.1)) and the ratio P(0.1)/PI(max) were assessed prior to and after treatment including NIV. Baseline data and changes at follow-up were used to evaluate their predictive value for long-term survival. RESULTS: Overall, median (quartiles) P(0.1) was 177.0 (109.2;287.0) %pred, PI(max) 35.0 (24.0;47.0) %pred, and P(0.1)/PI(max) 564.0 (275.7;1082.3) %pred. In multivariate analyses, P(0.1) was related to airflow obstruction, lung hyperinflation, haemoglobin (Hb) and leukocytes, and PI(max) to airflow obstruction and hyperinflation (p<0.05 each). All-cause mortality during follow-up (median 31.6 months) was 31.5%. Survival was associated with age, body-mass index (BMI), lung function, leukocytes, Hb, PI(max), P(0.1) and P(0.1)/PI(max) (p<0.01 each, univariate). Among these multivariate Cox regression identified age, BMI, FEV(1), leukocytes and P(0.1)/PI(max) as independent predictors (p<0.05 each). Furthermore, the decrease of P(0.1)/PI(max) at follow-up was associated with improved survival in patients with high baseline P(0.1)/PI(max) (>50th or 75th percentile; p<0.05). CONCLUSIONS: In patients with CHRF and current NIV therapy, P(0.1)/PI(max) was an independent predictor of long-term survival, in addition to previously established risk factors. Moreover, a decrease in P(0.1)/PI(max) after treatment including NIV was associated with an improved survival in patients with high baseline P(0.1)/PI(max) values.     

The effects of hydralazine on exercise capacity in pulmonary hypertension secondary to chronic obstructive pulmonary disease

Vasodilator therapy of pulmonary hypertension has been shown to improve hemodynamics in some patients, but the clinical benefits of this therapy have not been evaluated. We studied 14 patients who had pulmonary hypertension secondary to chronic obstructive pulmonary disease to determine the effect of hydralazine treatment on hemodynamics and maximal exercise. Baseline exercise in these subjects showed an abnormal pattern of excessive tachycardia and low stroke volumes, and the stroke volume correlated inversely with the pulmonary vascular resistance during exercise (r = -0.61, p less than 0.05). After 48 h of hydralazine there were decreases in the mean pulmonary artery pressure (43 +/- 8 to 38 +/- 8 mmHg, p less than 0.06) and pulmonary vascular resistance (3.97 +/- 0.97 to 2.88 +/- 1.28 units, p less than 0.05) measured at maximal exercise, and the maximal cardiac output was increased (8.05 +/- 2.57 to 10.13 +/- 2.79 L/min, p less than 0.05), but there was no change in symptom-limited maximal oxygen consumption (747 +/- 266 to 752 +/- 244 ml/min, p = NS). Significant increases in resting and maximal exercise values of minute ventilation and mixed venous oxygen tension were also noted with hydralazine. Repeat exercise testing after 2 to 4 months of chronic hydralazine therapy demonstrated no change in symptom-limited maximal oxygen consumption. We conclude that vasodilator therapy with hydralazine, although hemodynamically efficacious, does not increase exercise capacity in patients with severe chronic obstructive pulmonary disease and secondary pulmonary hypertension.     

Long-term effects of hydralazine on ventilation and blood gas values in patients with chronic obstructive pulmonary disease and pulmonary hypertension

Hydralazine has been shown to increase minute ventilation, alveolar ventilation, and arterial partial pressure of oxygen (PaO2) after short-term administration in patients with chronic obstructive pulmonary disease and pulmonary hypertension. The effects of orally administered hydralazine on ventilation and blood gas values were evaluated after six to 18 months of treatment in 10 male patients who had demonstrated an increase in minute ventilation after 24 hours of treatment. Hydralazine was administered at a dose of 200 mg per day during the initial 24 hours and in doses ranging from 40 mg per day to 200 mg per day during long-term therapy. Following 24 hours of treatment, a statistically significant increase in minute ventilation, alveolar ventilation, and PaO2, and reduction in arterial partial pressure of carbon dioxide (PaCO2) were seen both at rest and during exercise. After six to 18 months of hydralazine therapy, the increase in minute ventilation at rest persisted when compared with the pre-hydralazine value (15.3 +/- 1.3 liters/minute versus 13.1 +/- 1.1 liters/minute; p less than 0.05). The improvement in PaO2 at rest continued relative to the pre-hydralazine value (70.9 +/- 3.2 mm Hg versus 65.1 +/- 3.0 mm Hg, p less than 0.05) as did the PaO2 during exercise (60.3 +/- 3.5 mm Hg versus 53.3 +/- 2.0 mm Hg; p less than 0.05). The reduction in PaCO2 at rest persisted compared with the pre-hydralazine value (41.2 +/- 2.4 mm Hg versus 47.0 +/- 3.0 mm Hg; p less than 0.05) as did the PaCO2 during exercise (44.0 +/- 2.8 mm Hg versus 48.0 +/- 2.8 mm Hg; p less than 0.05). No significant changes in minute ventilation, PaO2, or PaCO2 were seen at rest or during exercise, when re-measured after six to 18 months in an age- and sex-matched control group of 10 patients who did not receive hydralazine. These results demonstrate that the short-term effects of hydralazine on ventilation and blood gas values persisted after six to 18 months of treatment in this sample of patients, some of whom received doses less than 200 mg per day.     

Effects of noninvasive proportional assist vs pressure support ventilation on respiratory work in chronic obstructive pulmonary disease patients with hypercapnia

正Objective To investigate the effect of noninvasive proportional assist ventilation(PAV)on respiratory work in chronic obstructive pulmonary disease(COPD)patients,in comparison with noninvasive pressure support ventilation(PSV).Methods Ten severe COPD patients     

Diffference between mouth and esophageal occlusion pressure during CO2 rebreathing in chronic obstructive pulmonary disease.

During CO2 rebreathing, we measured the pressures generated at the mouth and in the esophagus during the first 0.1 sec of inspiratory effort against a closed airway in 6 normal subjects and 6 patients with chronic obstructive lung disease. Normal subjects showed similar reponses to CO2 in terms of both mouth pressure and esophageal pressure. Patients' responses at the mouth to CO2 were decreased compared to those of normal subjects, but the responses in the esophagus were not significantly different. The patients demonstrated a greater response of occlusion pressure measured in the esophagus than at the mouth. In patients with altered mechanical properties of the lung, the change in mouth occlusion pressure might be influenced by problems of equalization of pressure within the airways due to unequal time constants, by problems of regional differences in pressure gradients over the pleural surface, or both. Esophageal pressure during airway occlusion 100 msec after the onset of inspiration may be better measure of respiratory drive than mouth pressure in patients with intrinsic increase of airway resistance.     

Familial aspects of ventilatory control in patients with chronic obstructive pulmonary disease

To determine whether abnormal chemical drives to breathe in patients with chronic obstructive pulmonary disease (COPD) antedate the development of chronic CO2 retention, we measured ventilatory and P0.1 responses to hypercapnia and hypoxia in 14 such patients and 23 of their normal adult offspring. Hypoxic responses in the patients were positively correlated with the mean hypoxic responses of their offspring. Neither the hypercapnic responses nor the resting breathing patterns of the patients were related to those of their offspring. Hypoxic response was lower in offspring of hypercapnic patients than in offspring of normocapnic patients. Blunt hypoxic responses in patients with COPD are influenced by familial factors and may represent a premorbid "risk factor" in the development of CO2 retention in this disease. This does not appear to be true for hypercapnic response or breathing pattern.     

Effects of dipyridamole on the hypoxemic pulmonary hypertension of patients with chronic obstructive pulmonary disease

Based on the hypothesis that blood platelets contribute to the pathogenesis of hypoxemic pulmonary hypertension in patients with chronic obstructive pulmonary disease (COPD), the effect of a prolonged treatment with dipyridamole, a platelet-inhibiting drug, on hypoxemic pulmonary hypertension was evaluated in a double-blind cross-over study. Eight patients with COPD, pulmonary hypertension [mean systolic pressure 52.2 +/- (SD) 9.7 mm Hg; mean diastolic pressure 25.8 +/- (SD) 6.8 mm Hg] and shortened platelet regeneration time [mean 5.2 +/- (SD) 1.2 days] received, in a cross-over random sequence, the following two 3-month treatments: (a) dipyridamole 100 mg and acetylcysteine 100 mg every 6 h; (b) acetylcysteine, 100 mg every 6 h. Dipyridamole significantly prolonged the platelet regeneration time [mean 6.5 +/- (SD) 1.0 days; p less than 0.05]. There was no significant effect on diastolic pulmonary pressure. However, systolic pressure was significantly (p less than 0.05) lower after dipyridamole [46.8 +/- (SD) 16 mm Hg] than after placebo [56.1 +/- (SD) 14 mm Hg]. These results suggest that dipyridamole can slow the progression of hypoxemic pulmonary hypertension in patients with COPD.     

Haemodynamic response to intravenous hydralazine in patients with pulmonary hypertension.

The acute pulmonary and systemic haemodynamic response to low (0.15 mg/kg) and high (0.30 mg/kg) doses of intravenous hydralazine was evaluated in 26 consecutive patients with severe pulmonary hypertension due to cor pulmonale (nine patients), primary pulmonary hypertension (11 patients), or pulmonary embolism (six patients). Hydralazine did not cause a significant change in pulmonary arterial resistance or pressure in any group but produced a significant reduction in systemic resistance, which correlated with plasma concentration, and a significant increase in pulmonary blood flow index in all groups. Ten patients who experienced a reduction in pulmonary arterial resistance of at least 5 U X m2 after administration of hydralazine had higher initial values for pulmonary arterial resistance and systemic resistance and a lower pulmonary blood flow index than those who did not respond. Maintenance oral hydralazine treatment during nine to 36 months of follow up did not seem to affect symptoms or mortality. These results indicate that hydralazine has limited value in acutely reducing pulmonary arterial pressure or affecting clinical outcome in patients with pulmonary hypertension.     

Effect of salmeterol on the ventilatory response to exercise in chronic obstructive pulmonary disease.

This study examined the effects of bronchodilator-induced reductions in lung hyperinflation on breathing pattern, ventilation and dyspnoea during exercise in chronic obstructive pulmonary disease (COPD). Quantitative tidal flow/volume loop analysis was used to evaluate abnormalities in dynamic ventilatory mechanics and their manipulation by a bronchodilator. In a randomised double-blind crossover study, 23 patients with COPD (mean +/- SEM forced expiratory volume in one second 42 +/- 3% of the predicted value) inhaled salmeterol 50 microg or placebo twice daily for 2 weeks each. After each treatment period, 2 h after dose, patients performed pulmonary function tests and symptom-limited cycle exercise at 75% of their maximal work-rate. After salmeterol versus placebo at rest, volume-corrected maximal expiratory flow rates increased by 175 +/- 52%, inspiratory capacity (IC) increased by 11 +/- 2% pred and functional residual capacity decreased by 11 +/- 3% pred. At a standardised time during exercise, salmeterol increased IC, tidal volume (VT), mean inspiratory and expiratory flows, ventilation, oxygen uptake (VO2) and carbon dioxide output. Salmeterol increased peak exercise endurance, VO2 and ventilation by 58 +/- 19, 8 +/- 3 and 12 +/- 3%, respectively. Improvements in peak VO2 correlated best with increases in peak VT; increases in peak VT and resting IC were interrelated. The reduction in dyspnoea ratings at a standardised time correlated with the increased VT. Mechanical factors play an important role in shaping the ventilatory response to exercise in chronic obstructive pulmonary disease. Bronchodilator-induced lung deflation reduced mechanical restriction, increased ventilatory capacity and decreased respiratory discomfort, thereby increasing exercise endurance.     

无创正压通气对慢性阻塞性肺疾病合并肺动脉高压患者疗效分析

目的探讨无创正压通气对慢性阻塞性肺疾病(COPD)合并肺动脉高压(PH)患者的治疗作用。方法入选对象为本科室病房2014年10月至2016年1月收治入院经治疗达到COPD稳定期且合并肺动脉高压的136例患者。所有患者通过超声心动图检查收缩期肺动脉压(sPAP)40 mm Hg。136例患者中男121例,女15例,平均年龄(60.3±11.3)岁,随机分为无创正压通气(NPPV)组和常规治疗组。比较两组治疗前后FEV1/预计值、氧合指数、PCO_2、sPAP、BNP指标的差异,并进行sPAP与氧合指数、PCO_2、BNP、FEV1/预计值的相关性分析。结果 (1)NPPV组治疗后与治疗前以及与常规组治疗后在氧合指数、PCO_2、BNP较前有明显改善(P0.05),而FEV1/预计值、sPAP无统计学差异(P0.05)。常规组治疗前后无统计学意义(P0.05);(2)根据sPAP值分为A组(40 mm HgsPAP≤60 mm Hg)以及B组(sPAP60 mm Hg)进行分层研究显示:常规组治疗前后对应A、B亚组在FEV1/预计值、氧合指数、PCO_2、BNP、sPAP均无统计学差异(P0.05)。NPPV治疗组A组治疗后患者氧合指数、PCO_2、BNP、sPAP较治疗前及常规组A组治疗后均有改善(P0.05);B组治疗后在氧合指数、PCO2、BNP较治疗前及常规组B组治疗后有明显改善(P0.05),而FEV1/预计值、sPAP无统计学差异(P0.05);(3)sPAP与氧合指数呈负相关,与BNP呈正相关(P0.05)。结论无创正压通气治疗老年慢性阻塞性肺疾病合并轻度肺动脉高压患者安全有效,可以减低肺动脉高压。     

Nocturnal pulmonary hypertension in patients with chronic obstructive pulmonary disease.

Oxygen desaturation occurs during sleep in some patients with COPD. To investigate the effects of these hypoxemic episodes on the pulmonary vasculature, we studied four patients with our routine polysomnographic techniques and simultaneously recorded pulmonary artery pressure. In all four subjects, nocturnal episodes of desaturation were accompanied by elevations in the pulmonary artery pressure. Low flow oxygen abolished the drops in arterial oxygen saturation (but not the breathing abnormalities) and no elevations in the PA pressure were observed. We postulate that in some COPD patients these initially transient events may lead to sustained pulmonary hypertension and cor pulmonale. Nocturnal oxygen therapy may be indicated in more patients than previously suspected and may prevent the development of cor pulmonale.     

Effect of negative pressure ventilation on ventilatory muscle endurance in patients with severe chronic obstructive pulmonary disease.

We studied five men with chronic obstructive pulmonary disease (COPD) (mean age, 65 +/- SEM 2 yr; FEV1, 0.68 +/- 0.08 L; and FEV1/FVC, 38 +/- 2%) to determine the relationship between ventilatory muscle endurance (VME) and ventilatory muscle rest (VMR) elicited by negative-pressure ventilation (NPV). VME was measured as the maximal sustainable ventilation (MSVC) that the subjects could maintain for 12 min. Prior to therapy, MSVC for the subjects was 25.0 +/- 3.6 L/min. During the therapy phase, subjects received 4 wk of daily "in-hospital-supervised" NPV therapy (4 h/day). While subjects received therapy, we quantified VMR by (1) the percentage of breaths that were "in synchrony" and by (2) the percentage of breaths showing "turn-off" of the diaphragmatic EMG signal (EMGdl). During the therapy sessions, 93 +/- 2% of breaths were in synchrony, whereas 66 +/- 11% showed EMGdl turn-off. During post-therapy testing, an increase in MSVC was noted in each of the subjects; the mean increase was 4.0 +/- 1.3 L/min (p less than 0.05), which represented an increase of 16 +/- 4% over pretherapy values. Increases in MSVC were highly correlated with both the percentage of in-synchrony breaths (r = 0.96, p less than 0.01) and the percentage of breaths showing EMGdl turn-off (r = 0.92, p less than 0.02). However, NPV therapy elicited no other improvements in either clinical or laboratory measurements. Moreover, patients exhibited marked dyspnea with initiation and termination of daily NPV therapy.(ABSTRACT TRUNCATED AT 250 WORDS)     

Hyperoxic-induced hypercapnia in stable chronic obstructive pulmonary disease

We investigated the mechanism of hyperoxic-induced hypercapnia in 17 stable patients with moderate to severe chronic obstructive pulmonary disease (mean FEV1 = 0.95 L and FVC = 2.43 L). Ventilatory and mouth occlusion pressure (P0.1) responses to hypercapnia and hypoxia were measured with standard rebreathing techniques. In a randomized, single-blind fashion, we studied the effect of 15 min of hyperoxia or air on transcutaneous carbon dioxide (PtcCO2), CO2 production (VCO2), total minute ventilation (VE), and calculated dead space to tidal volume ratio (VD/VT). With O2, the PtcCO2 (p less than 0.01) and VD/VT (p less than 0.02) increased. The change in PtcCO2 with O2 was not significantly related to the indices of respiratory drive, nor to the baseline PtcCO2 or SaO2, but was related to the FEV1 (p less than 0.05). The O2 caused a slight decrease in mean VE and mean VCO2, but the effects in individual patients were variable. Both substantial increases or decreases in VE (delta VE) occurred, but these were accompanied by changes in VCO2 (delta VCO2) in the same direction. The effect of changes in VE on PaCO2 is shown to be almost completely cancelled by the concomitant changes in VCO2. Thus, the major portion of the change in PaCO2 was due to changes in VD/VT. We conclude that hyperoxic-induced hypercapnia is primarily due to impairment in gas exchange rather than to depression of ventilation. A reduced FEV1 appears to be a significant risk factor, whereas indices of respiratory drive are not likely to play a major role.     

Effect of chlormadinone acetate on ventilatory control in patients with chronic obstructive pulmonary disease

Twelve patients with chronic obstructive pulmonary disease (COPD) were studied to determine the effect of ventilatory stimulation with chlormadinone acetate (CMA), a potent synthetic progesterone, on chemical and neuromechanical respiratory controls and pulmonary gas exchange. Using a randomized, double-blind, cross-over trial, 1 wk of CMA therapy caused a significant reduction in arterial CO2 tension (Paco2) by 4.6 +/- 0.6 (SE) mmHg. This Paco2 fall was associated with increased minute ventilation (Vl), tidal volume (VT), and mean inspiratory flow (VT/Tl). During CMA administration, occlusion pressure response to CO2 with and without inspiratory flow-resistive loading increased significantly (p less than 0.01) over that during placebo administration, whereas ventilatory response to CO2 did not. In addition, normocapnic ventilatory and occlusion pressure response to hypoxia were significantly elevated (p less than 0.01) during CMA therapy. Furthermore, the degree of load compensation, which was assessed by the ratio of the loaded to unloaded slope in the occlusion pressure response to CO2, increased in all subjects after CMA administration. These results indicate that CMA augments not only the respiratory neuromuscular response to hypercapnia and hypoxia, but also flow-resistive load compensation in patients with COPD, and it may provide support for the use of CMA in patients who are able to decrease their Paco2 with this agent.     

阿托伐他汀治疗慢性阻塞性肺疾病合并肺动脉高压的临床研究

目的 分析慢性阻塞性肺疾病(COPD)继发的肺动脉高压(PAH)与炎症反应的相关性,研究阿托伐他汀对COPD合并PAH患者的治疗作用及可能机制.方法 收集我科稳定期单纯性COPD患者(40例),COPD合并PAH患者(45例)血清及呼出气冷凝液(EBC)标本,并常规行肺功能、动脉血气分析、超声心动图、6分钟步行距离(6MWD)、肝肾功能检测.乳胶增强透射免疫比浊法测定血清及EBC中高敏C-反应蛋白(hs-CRP).ELISA方法检测血清及EBC中肿瘤坏死因子-α(TNF-α).将稳定期COPD合并PAH患者随机分成治疗组(23例)和对照组(22例),对照组给予常规治疗,治疗组加用阿托伐他汀20 mg/d口服,6个月后观察两组的肺动脉压力、动脉血气分析、肺功能、6MWD、肝肾功能、血清及EBC中hs-CRP、TNF-α水平.结果 与单纯性COPD组相比,COPD合并PAH组PaO2、6MWD明显降低(P值均＜0.05),血清及EBC中hs-CRP、TNF-α水平明显增高(P值均＜0.05),且PaO2、6MWD与肺动脉收缩压(PASP)呈负相关(r=-0.472,P＜0.05;r=-0.435,P＜0.05),血清及EBC中hs-CRP、TNF-α均与PASP呈正相关(r=0.350～0.598,P值均＜0.05),6个月后,治疗组PASP力比同组治疗前和对照组治疗后均有明显降低(P＜0.05),差异有统计学意义;治疗组PaO2、6MWD比同组治疗前及对照组治疗后均有明显增高(P＜0.05),差异有统计学意义;两组血清及EBC中hs-CRP、TNF-α均明显降低(P值均＜0.05),但治疗组较对照组降低更明显,差异有统计学意义.结论全身及肺脏局部炎症反应可能参与了COPD继发的PAH形成过程.阿托伐他汀可降低COPD合并PAH患者肺动脉压力,改善动脉血氧分压及运动耐量,其机制可能与抑制全身及肺脏局部炎症反应有关.     

Ventilatory and occlusion pressure responses to hypercapnia in patients with chronic renal failure

Little is known of the effect of chronic renal failure (CRF) on ventilatory regulation. In 38 subjects (19 healthy, 19 with CRF before and after dialysis), we performed measurements of ventilation (VE) and occlusion pressure (P0.1) while the subjects were breathing air and hypercapnic gas mixtures. The results have shown that (1) during air ventilation, CRF patients exhibited lower values of VE and P0.1, which returned to normal after dialysis; (2) during hypercapnic ventilation, CRF patients had the same response as healthy subjects for VE but higher P0.1; hemodialysis induced an upward shift of the CO2 response curve in CRF patients. A twofold mechanism is probably involved: pulmonary edema, which reduces lung elasticity, and neuromuscular hypoexcitability, both implying a stronger central command.     

慢性阻塞性肺疾病患者炎症细胞因子与肺通气功能的相关研究

目的　探讨慢性阻塞性肺疾病 (COPD)患者肺通气功能改变与炎症因子变化之间的关系。方法　稳定期COPD和慢性支气管炎 (简称慢支 )患者各 8例 ,,另有 8名健康者作为对照 ,进行肺功能检查 ,并经支气管肺泡灌洗获取肺泡巨噬细胞进行培养 ,采用酶联免疫吸附 (ELISA)方法测定大肠杆菌内毒素 (LPS)刺激后上清液中白细胞介素 8(IL 8)、IL 1β、IL 6和肿瘤坏死因子α(TNF α)的浓度 ,细胞因子之间相关性采用Pearson相关阵分析 ,肺功能值与细胞因子相关性采用多元后退回归法分析。结果　 (1)肺泡巨噬细胞释放IL 8:加入LPS后COPD组为 [(43± 2 7) μg/L和 (5 7± 41) μg/L],与正常对照组 [(13± 10 ) μg/L和 (2 0± 13 ) μg/L) ]比较差异有显著性 (P <0 .0 5 ) ;与慢支组 [(2 9± 2 1)μg/L和 (3 2± 2 3 ) μg/L]比较差异有显著性 (P >0 .0 5 )。 (2 )加入LPS前、后 ,COPD组、慢支组和正常对照组肺泡巨噬细胞释放IL 1β分别为 [(5 0± 41)ng/L、(94± 5 9)ng/L、(3 7± 3 2 )ng/L、(2 2 5± 10 8)ng/L、(15 3± 175 )ng/L、(70± 3 7)ng/L],与IL 8的释放呈正相关 (P <0 .0 5 ) ;三组肺泡巨噬细胞在LPS刺激后释放TNF α分别为 [(12 3 8± 679)ng/L、(3 0 88± 2 879)ng/L、(13 3 2± 1846)ng/L],与IL 1β呈正相