Hyperoxia during one lung ventilation: Inflammatory and oxidative responses

被引:39
作者
Fisher, Alicia Olivant [1 ]
Husain, Kamran [2 ]
Wolfson, Marla R. [3 ]
Hubert, Terrence L. [3 ]
Rodriguez, Elena [1 ]
Shaffer, Thomas H. [1 ,3 ]
Theroux, Mary C. [1 ,2 ,3 ]
机构
[1] Nemours Alfred I duPont Hosp Children, Nemours Ctr Pediat Lung Res, Wilmington, DE 19803 USA
[2] Nemours Alfred I duPont Hosp Children, Dept Anesthesiol & Crit Care, Wilmington, DE 19803 USA
[3] Temple Univ, Sch Med, Dept Physiol, Philadelphia, PA 19122 USA
基金
美国国家卫生研究院;
关键词
single-lung ventilation; thoracic surgery; acute lung injury; ISCHEMIA-REPERFUSION INJURY; PULMONARY OXYGEN-TOXICITY; MECHANICAL VENTILATION; RESPIRATORY-DISTRESS; STRESS; ALVEOLAR; MODEL; RESECTION; DAMAGE; GAS;
D O I
10.1002/ppul.22517
中图分类号
R72 [儿科学];
学科分类号
100202 ;
摘要
Background It is common practice during one lung ventilation (OLV) to use 100% oxygen, although this may cause hyperoxia- and oxidative stress-related lung injury. We hypothesized that lower oxygen (FiO2) during OLV will result in less inflammatory and oxidative lung injury and improved lung function. Methods Twenty pigs (8.88?+/-?0.84?kg; 38?+/-?4.6 days) were assigned to either the hyperoxia group (n?=?10; FiO2?=?100%) or the normoxia group (n?=?10; FiO2?<?50%). Both groups were subjected to 3?hr of OLV. Blood samples were tested for pro-inflammatory cytokines and lung tissue was tested for these cytokines and oxidative biomarkers. Results There were no differences between groups for partial pressure of CO2, tidal volume, end-tidal CO2, plasma cytokines, or respiratory compliance. Total respiratory resistance was greater in the hyperoxia group (P?=?0.02). There were higher levels of TNF-a, IL-1 beta, and IL-6 in the lung homogenates of the hyperoxia group than in the normoxia group (P?=?0.01, 0.001, and 0.001, respectively). Myeloperoxidase and protein carbonyls (PC) were higher (P?=?0.03 and P?=?0.01, respectively) and superoxide dismutase (SOD) was lower in the lung homogenates of the hyperoxia group (P?=?0.001). Conclusion Higher myeloperoxidase, PC, and cytokine levels, and lower SOD availability indicate a greater degree of injury in the lungs of the hyperoxia animals, possibly from using 100% oxygen. In this translational study using a pig model, FiO2?=?50% during OLV reduced hyperoxic injury and improved function in the lungs. Pediatr Pulmonol. 2012. 47:979986. (c) 2012 Wiley Periodicals, Inc.
引用
收藏
页码:979 / 986
页数:8
相关论文
共 37 条
[1]  
[Anonymous], OPEN ANESTHESIOL J
[2]   Molecular mechanisms of hyperoxia-induced acute lung injury [J].
Bhandari, Vineet .
FRONTIERS IN BIOSCIENCE-LANDMARK, 2008, 13 :6653-6661
[3]   Hyperoxia causes angiopoietin 2-mediated acute lung injury and necrotic cell death [J].
Bhandari, Vineet ;
Choo-Wing, Rayman ;
Lee, Chun G. ;
Zhu, Zhou ;
Nedrelow, Jonathan H. ;
Chupp, Geoffrey L. ;
Zhang, Xucher ;
Matthay, Michael A. ;
Ware, Lorraine B. ;
Homer, Robert J. ;
Lee, Patty J. ;
Geick, Anke ;
de Fougerolles, Antonin R. ;
Elias, Jack A. .
NATURE MEDICINE, 2006, 12 (11) :1286-1293
[4]   Cytokines in tolerance to hyperoxia-induced injury in the developing and adult lung [J].
Bhandari, Vineet ;
Elias, Jack A. .
FREE RADICAL BIOLOGY AND MEDICINE, 2006, 41 (01) :4-18
[5]   PERMISSIVE HYPERCAPNIA IN ACUTE RESPIRATORY-FAILURE [J].
BIDANI, A ;
TZOUANAKIS, AE ;
CARDENAS, VJ ;
ZWISCHENBERGER, JB .
JAMA-JOURNAL OF THE AMERICAN MEDICAL ASSOCIATION, 1994, 272 (12) :957-962
[6]  
Brodsky Jay B, 2005, Thorac Surg Clin, V15, P1, DOI 10.1016/j.thorsurg.2004.08.005
[7]  
Carden DL, 2000, J PATHOL, V190, P255, DOI 10.1002/(SICI)1096-9896(200002)190:3<255::AID-PATH526>3.0.CO
[8]  
2-6
[9]   Oxidative stress during 1 lung ventilation [J].
Cheng, Ya-Jung ;
Chan, Kuang-Cheng ;
Chien, Chiang-Ting ;
Sun, Wei-Zen ;
Lin, Chen-Jung .
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 2006, 132 (03) :513-518
[10]   Oxidative stress precedes peak systemic inflammatory response in pediatric patients undergoing cardiopulmonary bypass operation [J].
Christen, S ;
Finckh, B ;
Lykkesfeldt, J ;
Gessler, P ;
Frese-Schaper, M ;
Nielsen, P ;
Schmid, ER ;
Schmitt, B .
FREE RADICAL BIOLOGY AND MEDICINE, 2005, 38 (10) :1323-1332