募集手法根据急性肺损伤的病因调节上皮细胞和内皮细胞的反应。

Recruitment maneuvers modulate epithelial and endothelial cell response according to acute lung injury etiology.

机构信息

1Laboratory of Pulmonary Investigation, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. 2Laboratory of Experimental Surgery, Faculty of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. 3Laboratory of Cellular and Molecular Physiology, Carlos Chagas Filho Biophysics Institute, Federal University of Rio de Janeiro, Rio de Janeiro, Brazil. 4Department of Pathology, School of Medicine, University of São Paulo, São Paulo, Brazil. 5Rio de Janeiro Federal Institute of Education, Science and Technology, Rio de Janeiro, Brazil. 6Pulmonary Engineering Group, Department of Anesthesiology and Intensive Care Therapy, University Hospital Carl Gustav Carus, Dresden University of Technology, Dresden, Germany. 7IRCCS AOU San Martino-IST, Department of Surgical Sciences and Integrated Diagnostics, University of Genoa, Genoa, Italy. 8University of Minnesota, Minnesota Regions Hospital, Pulmonary and Critical Care Medicine, Minneapolis-St Paul, MN.

出版信息

Crit Care Med. 2013 Oct;41(10):e256-65. doi: 10.1097/CCM.0b013e31828a3c13.

DOI:10.1097/CCM.0b013e31828a3c13

PMID:23887231

Abstract

OBJECTIVE

To investigate the effects of the rate of increase in airway pressure and duration of lung recruitment maneuvers in experimental pulmonary and extrapulmonary acute lung injury.

DESIGN

Prospective, randomized, controlled experimental study.

SETTINGS

University research laboratory.

SUBJECTS

Fifty adult male Wistar rats.

INTERVENTIONS

Acute lung injury was induced by Escherichia coli lipopolysaccharide either intratracheally (pulmonary acute lung injury) or intraperitoneally (extrapulmonary acute lung injury). After 24 hours, animals were assigned to one of three different recruitment maneuvers, targeted to maximal airway pressure of 30 cm H2O: 1) continuous positive airway pressure for 30 seconds (CPAP-30); 2) stepwise airway pressure increase (5 cm H2O/step, 8.5 s at each step) over 51 seconds (STEP-51) to achieve a pressure-time product similar to that of CPAP-30; and 3) stepwise airway pressure increase (5 cm H2O/step, 5 s at each step) over 30 seconds with maximum pressure sustained for a further 30 seconds (STEP-30/30).

MEASUREMENTS AND MAIN RESULTS

All recruitment maneuvers reduced static lung elastance independent of acute lung injury etiology. In pulmonary acute lung injury, CPAP-30 yielded lower surfactant protein-B and higher type III procollagen expressions compared with STEP-30/30. In extrapulmonary acute lung injury, CPAP-30 and STEP-30/30 increased vascular cell adhesion molecule-1 expression, but the type of recruitment maneuver did not influence messenger ribonucleic acid expression of receptor for advanced glycation end products, surfactant protein-B, type III procollagen, and pro-caspase 3.

CONCLUSIONS

CPAP-30 worsened markers of potential epithelial cell damage in pulmonary acute lung injury, whereas both CPAP-30 and STEP-30/30 yielded endothelial injury in extrapulmonary acute lung injury. In both acute lung injury groups, recruitment maneuvers improved respiratory mechanics, but stepwise recruitment maneuver without sustained airway pressure appeared to associate with less biological impact on lungs.

摘要

目的

探讨气道压力增加率和肺复张手法持续时间对实验性肺内和肺外急性肺损伤的影响。

设计

前瞻性、随机、对照实验研究。

地点

大学研究实验室。

对象

50 只成年雄性 Wistar 大鼠。

干预措施

通过气管内（肺内急性肺损伤）或腹腔内（肺外急性肺损伤）给予大肠杆菌脂多糖诱导急性肺损伤。24 小时后，动物被分为三组不同的肺复张手法，目标气道压力均为 30cmH2O：1）持续气道正压 30 秒（CPAP-30）；2）逐步气道压力增加（每步 5cmH2O，8.5s），持续 51 秒，达到与 CPAP-30 相似的压力-时间乘积（STEP-51）；3）逐步气道压力增加（每步 5cmH2O，5s），持续 30 秒，然后最大压力再持续 30 秒（STEP-30/30）。

测量和主要结果

所有肺复张手法均降低了静态肺弹性，与急性肺损伤病因无关。在肺内急性肺损伤中，CPAP-30 与 STEP-30/30 相比，表面活性蛋白-B 的表达降低，III 型前胶原的表达升高。在肺外急性肺损伤中，CPAP-30 和 STEP-30/30 增加了血管细胞黏附分子-1 的表达，但肺复张手法的类型并不影响晚期糖基化终产物受体、表面活性蛋白-B、III 型前胶原和 pro-caspase3 的信使核糖核酸表达。