Hyperoxic ventilation exacerbates lung reperfusion injury

被引:14
作者
Ellman, PI [1 ]
Alvis, JS [1 ]
Tache-Leon, C [1 ]
Singh, R [1 ]
Reece, TB [1 ]
Kern, JA [1 ]
Tribble, CG [1 ]
Kron, IL [1 ]
机构
[1] Univ Virginia, Dept Cardiovasc Surg, Charlottesville, VA USA
关键词
D O I
10.1016/j.jtcvs.2005.06.037
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: It is well known that hyperoxia can be potentially harmful to the ventilated patient, although little is known about the potential effects in the setting of lung reperfusion. We hypothesized that hyperoxic ventilation at the time of reperfusion could worsen the effects of lung reperfusion injury. Methods: Using an ex vivo, blood perfused, isolated rabbit lung system, we evaluated the effects of hyperoxic (fraction of inspired oxygen = 100%, n = 10) versus normoxic (room air, n = 10) ventilation after 18 hours of cold ischemia. Lungs were ventilated and perfused for 2 hours. A control group was immediately perfused and ventilated with a fraction of inspired oxygen of 100%. Results: Lung wet/dry ratios dernonstrated lower tissue edema in the normoxic group compared with in the hyperoxic group (6.72 +/- 0.89 vs 7.62 +/- 1.14 [mean +/- standard error of the mean], P = .04). Lung ventilation was also significantly better in the non-noxic group versus the hyperoxic group (P-CO2 = 28.96 +/- 2.01 vs 36.68 +/- 3.20 mm Hg, P = .04). Conversely, lung oxygenation after 2 hours of reperfusion (normoxic group ventilated for the last 15 minutes on 100% fraction of inspired oxygen) was not significantly different between groups (P-O2 = 590.2 +/- 50.1 vs 499.6 +/- 67.5 mm Hg, P = .25). Conclusions: Ventilating lungs with 100% fraction of inspired oxygen at the time of reperfusion could increase the risk of lung reperfusion injury at the time of transplantation. Thus the patient should be ventilated with as low a fraction of inspired oxygen as possible to achieve adequate oxygen saturations during this critical reperfusion period.
引用
收藏
页码:1440 / 1445
页数:6
相关论文
共 24 条
[1]   ROLE OF XANTHINE-OXIDASE AND NEUTROPHILS IN ISCHEMIA-REPERFUSION INJURY IN RABBIT LUNG [J].
ADKINS, WK ;
TAYLOR, AE .
JOURNAL OF APPLIED PHYSIOLOGY, 1990, 69 (06) :2012-2018
[2]  
Bostek C C, 1989, AANA J, V57, P231
[3]   Ischemia-reperfusion-induced lung injury [J].
de Perrot, M ;
Liu, MY ;
Waddell, TK ;
Keshavjee, S .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2003, 167 (04) :490-511
[4]   Ischemia-reperfusion injury after lung transplantation increases risk of late bronchiolitis obliterans syndrome [J].
Fiser, SM ;
Tribble, CG ;
Long, SM ;
Kaza, AK ;
Kern, JA ;
Jones, DR ;
Robbins, MK ;
Kron, IL .
ANNALS OF THORACIC SURGERY, 2002, 73 (04) :1041-1047
[5]   OXYGEN-DEPENDENT LIPID-PEROXIDATION DURING LUNG ISCHEMIA [J].
FISHER, AB ;
DODIA, C ;
TAN, ZT ;
AYENE, I ;
ECKENHOFF, RG .
JOURNAL OF CLINICAL INVESTIGATION, 1991, 88 (02) :674-679
[6]  
FREEMAN BA, 1981, J BIOL CHEM, V256, P986
[7]   HYPEROXIC EXPOSURE IN HUMANS - EFFECTS OF 50-PERCENT OXYGEN ON ALVEOLAR MACROPHAGE LEUKOTRIENE-B4 SYNTHESIS [J].
GRIFFITH, DE ;
GARCIA, JGN ;
JAMES, HL ;
CALLAHAN, KS ;
IRIANA, S ;
HOLIDAY, D .
CHEST, 1992, 101 (02) :392-397
[8]   Normoxic cardiopulmonary bypass reduces oxidative myocardial damage and nitric oxide during cardiac operations in the adult [J].
Ihnken, K ;
Winkler, A ;
Schlensak, C ;
Sarai, K ;
Neidhart, G ;
Unkelbach, U ;
Mülsch, A ;
Sewell, A .
JOURNAL OF THORACIC AND CARDIOVASCULAR SURGERY, 1998, 116 (02) :327-334
[9]  
Ihnken K, 1996, Eur J Cardiothorac Surg, V10, P1127, DOI 10.1016/S1010-7940(96)80361-7
[10]   PULMONARY OXYGEN-TOXICITY [J].
JACKSON, RM .
CHEST, 1985, 88 (06) :900-905