Ⅱ型肺泡上皮细胞与急性肺损伤的研究进展

AECⅡ是肺泡壁的重要组成部分,也是ALI／ARDS发生、发展的重要参与者。AECⅡ可通过分泌炎症介质和促凝、抗凝因子参与ALl时全身炎症反应综合征和凝血反应失衡的形成。AECⅡ上Na^＋-K^＋-ATP酶活性以及数量的下调加重了．ALI时的肺水肿。肺组织内的AECII增生并转化为AECI以及间质细胞参与了肺损伤后的修复和纤维化的形成。而且,AECⅡ还具有免疫调节功能,参与肺组织内的防御反应。近年来研究发现,与AECⅡ相关的生物标志物SP—D和KL－6与ALI／ARDS肺损伤的严重程度及疾病的预后相关,但尚无对SP—D或KL－6与炎症反应相关性的研究。     

低潮气量通气改善猪急性肺损伤模型的脑组织氧合

背景本研究探讨在猪急性肺损伤（ALI）模型中应用不同潮气量对脑组织氧合和代谢的影响。我们假设在实验诱导急性肺损伤后,低潮气量（LT）机械通气能改善其脑组织的氧合和代谢。方法通过去除肺表面活性物质诱导实验性的急性肺损伤模型,10只母猪分别置于两种通气环境下：①6ml／kg的LT容量通气（LT组）;②12ml／kg的高潮气量机械通气（HT组）。分析气体交换、血流动力学、持续脑组织氧张力（ptiO2）、大脑微量透析和全身细胞因子等变量。诱导Au后,收集2、4和8小时的数值。主要观察指标为ptiO2的改变。组间比较采用t检验。P〈0．05为差异有显著性。结果基础状态和Au诱导后,未发现ptiO2存在组间差异;但是,HT组ptiO2在Au的4和8小时后显著降低。PaO2和PaCO2在任何记录时间点均无明显差异。大脑微量透析方面,HT组细胞外乳酸在2、4和8小时显示显著高水平。由于细胞因子的释放导致HT组IL-6和IL-8呈较高水平。结论在猪ALI模型中,与高潮气量通气比较,低潮气量保护性通气可以显著改善脑组织氧合和代谢。动脉氧合和大脑组织氧合存在分离现象。HT组的大脑组织氧合和代谢可能因更为突出的炎性反应而受损。     

Early application of the lung protective ventilation strategy at different stages in two ARDS patients

We experienced 2 patients with acute respiratory distress syndrome (ARDS) from pneumonia after intervention for subarachnoidal hemorrhage. We applied lung protective ventilation strategy (LPVS) on both cases: a tidal volume less than 6 ml x kg(-1) ideal body weight and PEEP at 10-15 cmH2O. Although etiology and degree of hypoxia were very similar in two patients when ARDS was diagnosed, clinical course was quite different. The patient in whom LPVS had been started on the 5th day of ARDS required mechanical ventilation of 23 days. In contrast, another patient in whom LPVS had been started on the 16th day of ARDS required mechanical ventilation of 219 days. PaCO2 during LPVS with permissive hypercapnia in the latter patient increased up to 161 mmHg but no adverse effect was observed. These cases suggest that early application of the LPVS may be important to improve respiratory outcomes of ARDS patients.     

Measurement of pressure-volume curves in patients on mechanical ventilation. Methods and significance

In critically ill patients measurements of pressure volume curves has been suggested as a method for assessing the severity of lung injury and for monitoring the evolution of the lung disease; it can also guide the ventilatory adjustments to optimize the mechanical ventilation. The static pressure-volume curves are impaired in acute respiratory distress syndrome (ARDS). The evaluation of the lower and upper inflection point on the pressure-volumes curves at the bedside of patients with acute respiratory failure means to apply a "protective ventilatory strategy". The combined application of positive end expiratory pressure (PEEP) to the level of alveolar recruitment and low tidal volume (< 6 ml/kg) ameliorates the lung function and decrease mortality in ARDS patients. Routine monitoring with continuous technique is easy and develops good therapeutic practice.     

Effect of detergent on alveolar particle clearance due to large tidal ventilation.

BACKGROUND--It has recently been shown that large tidal volume ventilation accelerates the alveolar clearance of insoluble particles and this may be related to accelerated surfactant evacuation from the alveolus into the airway. The aim of this study was to investigate if the effect of large tidal volume ventilation is modified in an experimental model of surfactant dysfunction. METHODS--Fluorescent latex particles of 0.63 microns diameter were administered in aerosol form to 30 rabbits during anaesthesia with thiopentone and mechanical ventilation. Six animals were killed immediately after aerosol administration in order to show the initial deposition of particles. Twenty four animals were divided into two groups and ventilated for three hours with either large tidal volume (mean tidal volume 30 ml/kg) or conventional ventilation (mean tidal volume 12.5 ml/kg). Six rabbits in each of the two groups were administered either the synthetic detergent dioctyl sodium sulphosuccinate in aerosol form or aerosolised vehicle. After the period of experimental ventilation the lungs were removed and dried in the expanded state. Particles in the alveolar region were counted with fluorescent microscopy in sections of the lung. RESULTS--Compared with the baseline group (mean (SD) 24.8 (9.9)) the count of residual alveolar particles was lower after large tidal volume ventilation in the absence of detergent aerosol (13.2 (6.5)). Particle count after large tidal volume ventilation and detergent treatment (23.3 (6.4)) was similar to that in the baseline group and to that in the groups exposed to conventional ventilation. CONCLUSIONS--The increase in alveolar clearance of insoluble particles caused by large tidal volume ventilation is inhibited by detergent aerosol. This might be due to reduced stability of the surfactant film after detergent aerosol.     

Lung protective ventilation strategies: have we applied them in trauma patients at risk for acute lung injury and acute respiratory distress syndrome?

Lung protective ventilation strategies for patients with acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are well documented, and many medical centers fail to apply these strategies in ALI/ARDS. The objective of this study was to determine if we apply these strategies in trauma patients at risk for ALI/ARDS. We undertook a retrospective review of trauma patients mechanically ventilated for > or = 4 days with an ICD-9 for traumatic pneumothorax, hemothorax, lung contusion, and/or fractured ribs admitted from May 1, 1999 through April 30, 2000 (Group 1), the pre-ARDS Network study, and from May 1, 2003 through April 30, 2004 (Group 2), the post-ARDS Network study. Tidal volume (VT)/kg admission body weight, VT/kg ideal body weight (IBW), and plateau and peak pressures were analyzed with respect to mortality. VT/Kg admission body weight and IBW were significantly reduced when comparing Group 1 with Group 2 (9.27 to 8.03 and 11.67 to 10.04, respectively). VT/kg IBW was greater (P < 0.01) for patients who died in Group 1 (13.81) compared with patients who lived (10.29) or died (9.89) in Group 2. Peak and plateau pressures were greater (P < 0.01) in patients who died in Group 1 than patients who lived or died in Group 2. A strict ARDS Network ventilation strategy (VT < 6 mL/kg) is not followed, rather a low plateau/peak pressure strategy is used, which is a form of lung protective ventilation.     

Acute respiratory distress syndrome--treatments today and tomorrow

Acute Respiratory Distress Syndrome (ARDS) is a life threatening condition. There are several randomized placebo controlled trials (RCT) that tested ventilated and non-ventilated patient managements. Among them, only ARMA trial that compared mortality and ventilator free-days between low tidal volume ventilation and conventional ventilation (6 and 12 ml x kg(-1) predicted body weight, respectively) showed differences (31.0% vs., 39.8%, P = 0.007 and 12 +/- 11 vs. 10 +/- 11 days, P = 0.007, respectively). The ALVEOLI trial testing high PEEP failed to show any benefit over the low tidal volume ventilation as control. Prone positioning may temporarily improve oxygenation, but does not affect mortality. High frequency oscillatory ventilation does not show strong evidence for mortality reduction over low tidal volume ventilation. Conservative strategy of fluid management after shock state increased ventilator-free days and ICU-free days without increasing adverse effects. Corticosteroids have been controversial. Methylprednisolone iv administration starting between 7 and 13 days of the onset of ARDS increased the number of ventilator-free days and shock-free days; whereas, methylprednisolone treatment starting more than two weeks after the onset of ARDS increased the risk of death. There are no RCTs that positively showed the improvement in mortality by using any therapeutic agent. Based on basic science studies, molecules that enhance epithelial and endothelial cell proliferation and the therapies targeting on septic pathophysiology would be the target for future strategies.     

Effect of mechanical ventilation on cytokine response to intratracheal lipopolysaccharide

BACKGROUND: Mechanical ventilation may cause lung injury through the excitation of an inflammatory response and the release of mediators, such as cytokines. The authors tested the hypothesis that intratracheal lipopolysaccharide amplifies the cytokine response to mechanical ventilation. METHODS: Rat lungs were intratracheally instilled with lipopolysaccharide followed by ex vivo mechanical ventilation for 2 h with low tidal volume of 7 ml/kg with 3 cm H2O positive end-expiratory pressure (PEEP), high tidal volume of 40 ml/kg with zero PEEP, medium tidal volume of 15 ml/kg with 3 cm H2O PEEP, or medium tidal volume and zero PEEP. RESULTS: In the absence of lipopolysaccharide, lung lavage concentrations of tumor necrosis factor and interleukin 1 beta but not macrophage inflammatory protein 2 were significantly higher in lungs ventilated at high tidal volume/zero PEEP than at low tidal volume. There was a marked increase in lavage tumor necrosis factor and macrophage inflammatory protein 2 concentrations in lungs ventilated at low tidal volume after exposure to intratracheal lipopolysaccharide at doses of 100 ng/ml or greater. However, in lungs ventilated at high tidal volume, this response to lipopolysaccharide was markedly reduced. In addition, the number of alveolar macrophages recovered in the lavage was significantly lower in lungs ventilated at high tidal volume. CONCLUSION: Ventilation strategy can modify lung cytokine responses to lipopolysaccharide, likely through an effect on the alveolar macrophage population.     

Sivelestat sodium hydrate was effective for ARDS in a patient suffering from chronic rheumatoid arthritis with acute exacerbation after failing to respond to high dose steroid pulse therapy

Sivelestat sodium hydrate (ELASPOL) was effective for ARDS in a fifty-year-old female patient suffering from chronic rheumatoid arthritis with acute exacerbation, after failing to respond to high dose steroid pulse therapy. In ICU, the patient had bilateral lung opacities, especially of the upper lobes, respiratory acidosis, hypercapnea (PaCO2 89 mmHg), and poor oxygenation (P/F ratio 193). High dose steroid pulse therapy had been performed, but oxygenation was not improved, and a low level of oxygenation (P/F ratio 155) persisted. Sivelestat was started two days after finishing the steroid pulse therapy. The butterfly shadow on chest X ray and impaired oxygenation were markedly improved from the third day of sivelestat administration. Respiratory support was terminated with P/F ratio 300. Plasma concentrations of SP-A and SP-D decreased after sivelestat administration, but concentration of KL-6 was still elevated. In this case, sivelestat was effective for ARDS in the patient not responding to steroid pulse therapy, and clinical finding and plasma concentrations of SP-A and SP-D were correlated well.     

Short-term cardiorespiratory effects of proportional assist and pressure-support ventilation in patients with acute lung injury/acute respiratory distress syndrome

BACKGROUND: Recent data indicate that assisted modes of mechanical ventilation improve pulmonary gas exchange in patients with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Proportional assist ventilation (PAV) is a new mode of support that amplifies the ventilatory output of the patient effort and improves patient-ventilator synchrony. It is not known whether this mode may be used in patients with ALI/ARDS. The aim of this study was to compare the effects of PAV and pressure-support ventilation on breathing pattern, hemodynamics, and gas exchange in a homogenous group of patients with ALI/ARDS due to sepsis. METHODS: Twelve mechanically ventilated patients with ALI/ARDS (mean ratio of partial pressure of arterial oxygen to fractional concentration of oxygen 190 +/- 49 mmHg) were prospectively studied. Patients received pressure-support ventilation and PAV in random order for 30 min while maintaining mean airway pressure constant. With both modes, the level of applied positive end-expiratory pressure (7.1 +/- 2.1 cm H2O) was kept unchanged throughout. At the end of each study period, cardiorespiratory data were obtained, and dead space to tidal volume ratio was measured. RESULTS: With both modes, none of the patients exhibited clinical signs of distress. With PAV, breathing frequency and cardiac index were slightly but significantly higher than the corresponding values with pressure-support ventilation (24.5 +/- 6.9 vs. 21.4 +/- 6.9 breaths/min and 4.4 +/- 1.6 vs. 4.1 +/- 1.3 l . min . m, respectively). None of the other parameters differ significantly between modes. CONCLUSIONS: In patients with ALI/ARDS due to sepsis, PAV and pressure-support ventilation both have clinically comparable short-term effects on gas exchange and hemodynamics.     

Innate immunity of surfactant protein A and D in urinary tract infection with uropathogenic Escherichia coli

Objective To investigate the role of surfactant protein (SP) - A and SP - D in urinary tract infection mouse model, and evaluate the effects of SP-A and SP-D absence on urinary tract infection. Methods SP-A and SP-D double knockout (SP-A/D KO) mice were made. SP-A/D KO and wild-type (WT) C57BL/6 female mice were used for this study. The expression of SP-A and SP-D in kidney was detected by immunohistochemistry (IHC). The levels of p - p38 and p38 protein in kidneys were measured by Western blotting. Uropathogenic Escherichia coli or buffer was delivered into the bladder of female mice. At 24 and 48 h after inoculation, CFU of Escherichia coli in the kidney and urine of the treated and control mice were measured. Histological, cellular and molecular analysis were performed by several methods of H/E staining, IHC and Western blotting. The effects of SP-A and SP-D on bacterial growth were studied in vitro. Results SP-A and SP-D in kidney were located in the proximal tubules and collecting tubules. Compared with WT mice, infected SP - A/D KO mice with UPEC had higher CFU in kidneys and urine at 24 h and 48 h, increased inflammatory cells infiltration in kidneys（P＜0.05）. Compared with WT mice, SP - A/D KO mice had higher p38 MAPK phosphorylation levels in kidneys（P＜0.05）. Growth of Escherichia coli was greatly inhibited by both SP-A and SP-D（P＜0.05）. Conclusions Both SP-A and SP-D are expressed in kidney. SP-A and SP-D can attenuate UTI induced by UPEC which may be through inhibiting bacterial growth and modulating renal inflammation.     

Short-term Cardiorespiratory Effects of Proportional Assist and Pressure-support Ventilation in Patients with Acute Lung Injury/Acute Respiratory Distress Syndrome

Background: Recent data indicate that assisted modes of mechanical ventilation improve pulmonary gas exchange in patients with acute lung injury (ALI)/acute respiratory distress syndrome (ARDS). Proportional assist ventilation (PAV) is a new mode of support that amplifies the ventilatory output of the patient effort and improves patient-ventilator synchrony. It is not known whether this mode may be used in patients with ALI/ARDS. The aim of this study was to compare the effects of PAV and pressure-support ventilation on breathing pattern, hemodynamics, and gas exchange in a homogenous group of patients with ALI/ARDS due to sepsis.

Methods: Twelve mechanically ventilated patients with ALI/ARDS (mean ratio of partial pressure of arterial oxygen to fractional concentration of oxygen 190 +/- 49 mmHg) were prospectively studied. Patients received pressure-support ventilation and PAV in random order for 30 min while maintaining mean airway pressure constant. With both modes, the level of applied positive end-expiratory pressure (7.1 +/- 2.1 cm H2O) was kept unchanged throughout. At the end of each study period, cardiorespiratory data were obtained, and dead space to tidal volume ratio was measured.

Results: With both modes, none of the patients exhibited clinical signs of distress. With PAV, breathing frequency and cardiac index were slightly but significantly higher than the corresponding values with pressure-support ventilation (24.5 +/- 6.9 vs. 21.4 +/- 6.9 breaths/min and 4.4 +/- 1.6 vs. 4.1 +/- 1.3 l [middle dot] min-1 [middle dot] m-2, respectively). None of the other parameters differ significantly between modes.     

Measurement of pulmonary status and surfactant protein levels during dexamethasone treatment of neonatal respiratory distress syndrome.

BACKGROUND: Early postnatal use of dexamethasone in infants with respiratory distress syndrome (RDS) has been shown effectively to improve pulmonary status and to allow early weaning off mechanical ventilation. However, the mechanisms to explain the beneficial effects of dexamethasone in ventilatory dependent preterm infants remain unclear. METHODS: A double blind, placebo controlled study was performed to determine the change in pulmonary ventilation of premature infants with RDS as a result of dexamethasone treatment, and to evaluate the effect of dexamethasone on the levels of surfactant-associated proteins A (SP-A) and D (SP-D) in the tracheal fluid from 34 premature infants with RDS and 29 control subjects. RESULTS: Dexamethasone treatment decreased fractional inspired oxygen concentration (FIO2), arterial carbon dioxide tension (PCO2), mean airway pressure (MAP), and facilitated successful weaning from mechanical ventilation. SP-A concentrations in the tracheal aspirates were increased at days 7 and 14, and SP-D concentrations were increased during the period from days 3 to 14 in the dexamethasone treated group compared with the control group. However, albumin levels in the tracheal aspirate samples were decreased after dexamethasone treatment over the period from days 3 to 14. There was an inverse correlation between PCO2 values and SP-A concentrations. CONCLUSIONS: These results suggest that early use of dexamethasone can improve pulmonary status and also increase SP-A and SP-D levels in the tracheal fluid in premature infants with RDS.     

Effects of surfactant replacement on alveolar overdistension and plasma cytokines in ventilator‐induced lung injury

Background: Overdistension of the lung causes ventilator‐induced lung injury (VILI) accompanied by surfactant abnormalities and inflammatory changes. We investigated the effects of surfactant replacement on overdistension of the terminal airspaces and plasma cytokine levels in VILI. Methods: VILI was induced by high‐pressure ventilation (HPV) in rats anesthetized with pentobarbital, followed by ventilation for 2 h in the maintenance mode (tidal volume=10 ml/kg, positive end‐expiratory pressure=7.5 cmH₂O) with or without surfactant replacement. The sizes of the terminal airspaces were determined after fixing the lungs at an airway pressure of 10 cmH₂O on deflation. Cytokine levels were assessed by enzyme‐linked immunosorbent assay. Results: The mean ratio of the largest terminal airspace size class (≥64,000 μm²) was increased from 13.4% to 32.0% by HPV (P<0.05). After maintenance‐mode ventilation, the ratio decreased to 16.1% with surfactant replacement (P<0.05), but increased to 44.6% without surfactant replacement (P<0.05). Mean macrophage inflammatory protein‐2 (MIP‐2) levels in the plasma increased from <0.02 to 6.9 ng/ml with HPV (P<0.05), and further increased to ≥11.8 ng/ml, regardless of surfactant replacement after maintenance‐mode ventilation. Similar tendencies were observed in the interleukin (IL)‐6 and IL‐10 levels. Tumor necrosis factor‐α levels were almost negligible during the experiment. Conclusion: In rats with VILI, surfactant replacement reversed overdistension of the terminal airspaces that may induce barotrauma, but not upregulation of MIP‐2, IL‐6, and IL‐10 within 2 h.     

Protective ventilation influences systemic inflammation after esophagectomy: a randomized controlled study

BACKGROUND: Esophagectomy induces a systemic inflammatory response whose extent has been recognized as a predictive factor of postoperative respiratory morbidity. The aim of this study was to determine the effectiveness of a protective ventilatory strategy to reduce systemic inflammation in patients undergoing esophagectomy. METHODS: The authors prospectively investigated 52 patients undergoing planned esophagectomy for cancer. Patients were randomly assigned to a conventional ventilation strategy (n = 26; tidal volume of 9 ml/kg during two-lung and one-lung ventilation; no positive end-expiratory pressure) or a protective ventilation strategy (n = 26; tidal volume of 9 ml/kg during two-lung ventilation, reduced to 5 ml/kg during one-lung ventilation; positive end-expiratory pressure 5 cm H2O throughout the operative time). RESULTS: Plasmatic levels of interleukin (IL)-1beta, IL-6, IL-8, and tumor necrosis factor alpha were measured perioperatively and postoperatively. Pulmonary function and postoperative evolution were also evaluated. Patients who received protective strategy had lower blood levels of IL-1beta, IL-6, and IL-8 at the end of one-lung ventilation (0.24 [0.15-0.40] vs. 0.56 [0.38-0.89] pg/ml, P < 0.001; 91 [61-117] vs. 189 [127-294] pg/ml, P < 0.001; and 30 [22-45] vs. 49 [29-69] pg/ml, P < 0.05, respectively) and 18 h postoperatively (0.18 [0.13-0.30] vs. 0.43 [0.34-0.54] pg/ml, P < 0.001; 54 [36-89] vs. 116 [78-208] pg/ml, P < 0.001; 16 [11-24] vs. 35 [28-53] pg/ml, P < 0.001, respectively). Protective strategy resulted in higher oxygen partial pressure to inspired oxygen fraction ratio during one-lung ventilation and 1 h postoperatively and in a reduction of postoperative mechanical ventilation duration (115 +/- 38 vs. 171 +/- 57 min, P < 0.001). CONCLUSION: A protective ventilatory strategy decreases the proinflammatory systemic response after esophagectomy, improves lung function, and results in earlier extubation.     

不同潮气量机械通气对创伤后急性呼吸窘迫综合征疗效的影响

目的探讨小潮气量(LTV)加呼气末正压(PEEP)机械通气(MV)治疗创伤后急性呼吸窘迫综合征(ARDS)的疗效。方法以18例常规潮气量(8～12ml/kg)MV为对照组,20例小潮气量(5～7ml/kg)加用PEEP的MV模式为观察组,比较两组间血气,RR、HR、MAP、CVP、呼吸机所致肺损伤(VILI)、多脏器功能不全(MODS)发生率及ARDS病死率。结果两组PaO2差异无显著性意义(P>0.05);观察组PaCO2高于对照组(P<0.05);观察组无VILI、MODS及死亡病例发生,对照组2例VILI、2例ARDS并发MODS死亡。结论在ARDS治疗中采用小潮气量加PEEP及允许范围内高碳酸血症(PHC)的保护性通气策略,可明显改善缺氧,减少VILI发生,从而降低其病死率。     

Alveolar Recruitment in Pulmonary and Extrapulmonary Acute Respiratory Distress Syndrome: Comparison Using Pressure-Volume Curve or Static Compliance

Background: Alveolar recruitment in response to positive end-expiratory pressure (PEEP) may differ between pulmonary and extrapulmonary acute respiratory distress syndrome (ARDS), and alveolar recruitment values may differ when measured by pressure-volume curve compared with static compliance.

Methods: The authors compared PEEP-induced alveolar recruitment in 71 consecutive patients identified in a database. Patients were classified as having pulmonary, extrapulmonary, or mixed/uncertain ARDS. Pressure-volume curves with and without PEEP were available for all patients, and pressure-volume curves with two PEEP levels were available for 44 patients. Static compliance was calculated as tidal volume divided by pressure change for tidal volumes of 400 and 700 ml. Recruited volume was measured at an elastic pressure of 15 cm H2O.

Results: Volume recruited by PEEP (10 +/- 3 cm H2O) was 223 +/- 111 ml in the pulmonary ARDS group (29 patients), 206 +/- 164 ml in the extrapulmonary group (16 patients), and 242 +/- 176 ml in the mixed/uncertain group (26 patients) (P = 0.75). At high PEEP (14 +/- 2 cmH2O, 44 patients), recruited volumes were also similar (P = 0.60). With static compliance, recruitment was markedly underestimated and was dependent on tidal volume (226 +/- 148 ml using pressure-volume curve, 95 +/- 185 ml for a tidal volume of 400 ml, and 23 +/- 169 ml for 700 ml; P < 0.001).     

Protective Ventilation Influences Systemic Inflammation after Esophagectomy: A Randomized Controlled Study

Background: Esophagectomy induces a systemic inflammatory response whose extent has been recognized as a predictive factor of postoperative respiratory morbidity. The aim of this study was to determine the effectiveness of a protective ventilatory strategy to reduce systemic inflammation in patients undergoing esophagectomy.

Methods: The authors prospectively investigated 52 patients undergoing planned esophagectomy for cancer. Patients were randomly assigned to a conventional ventilation strategy (n = 26; tidal volume of 9 ml/kg during two-lung and one-lung ventilation; no positive end-expiratory pressure) or a protective ventilation strategy (n = 26; tidal volume of 9 ml/kg during two-lung ventilation, reduced to 5 ml/kg during one-lung ventilation; positive end-expiratory pressure 5 cm H2O throughout the operative time).

Results: Plasmatic levels of interleukin (IL)-1[beta], IL-6, IL-8, and tumor necrosis factor [alpha] were measured perioperatively and postoperatively. Pulmonary function and postoperative evolution were also evaluated. Patients who received protective strategy had lower blood levels of IL-1[beta], IL-6, and IL-8 at the end of one-lung ventilation (0.24 [0.15-0.40] vs. 0.56 [0.38-0.89] pg/ml, P < 0.001; 91 [61-117] vs. 189 [127-294] pg/ml, P < 0.001; and 30 [22-45] vs. 49 [29-69] pg/ml, P < 0.05, respectively) and 18 h postoperatively (0.18 [0.13-0.30] vs. 0.43 [0.34-0.54] pg/ml, P < 0.001; 54 [36-89] vs. 116 [78-208] pg/ml, P < 0.001; 16 [11-24] vs. 35 [28-53] pg/ml, P < 0.001, respectively). Protective strategy resulted in higher oxygen partial pressure to inspired oxygen fraction ratio during one-lung ventilation and 1 h postoperatively and in a reduction of postoperative mechanical ventilation duration (115 +/- 38 vs. 171 +/- 57 min, P < 0.001).