Revisiting the essential role of oxygen in wound healing

被引:306
作者
Gordillo, GM [1 ]
Sen, CK [1 ]
机构
[1] Ohio State Univ, Dept Surg, Davis Heart & Lung Res Inst 512, Mol Med Lab, Columbus, OH 43210 USA
关键词
redox; hyperbaric oxygen therapy; oxygen toxicity; signal transduction; hyperoxia;
D O I
10.1016/S0002-9610(03)00211-3
中图分类号
R61 [外科手术学];
学科分类号
摘要
Hypoxemia, caused by disrupted vasculature, is a key factor that limits wound healing. Correcting hypoxemia through the administration of supplemental oxygen (O-2) can have significant beneficial impact on wound healing in the perioperative and outpatient settings. Beyond its role as a nutrient and antibiotic, O-2 may support vital processes such as angiogenesis, cell motility, and extracellular matrix formation. Recent discoveries highlight a novel aspect, addressing the role of O-2 in wound healing via the production of reactive oxygen species (ROS). Almost all wound-related cells possess specialized enzymes that generate ROS (including free radicals and H2O2) from O-2. Defect in these enzymes is associated with impaired healing. Low wound pO(2) is expected to compromise the function of these enzymes. At low concentrations, ROS serve as cellular messengers to support wound healing. The use of systemic hyperbaric 0, therapy presents potential advantages, as well as risks. There is evidence to suspect that the use of pressure and systemic pure O-2 may not be essential in wound care. Elimination of these factors by using sub-pure systemic O-2 under normobaric conditions may significantly minimize the risk of O-2 toxicity. Furthermore, opportunities to treat dermal wounds using topical O-2 therapy warrant further investigation. Given that many growth factors require ROS for their function, it is reasonable to assume that approaches to correct wound pO(2) will serve as an effective adjunct in treating chronic wounds. (C) 2003 Excerpta Medica, Inc. All rights reserved.
引用
收藏
页码:259 / 263
页数:5
相关论文
共 48 条
[1]  
Allen DB, 1997, ARCH SURG-CHICAGO, V132, P991
[2]   Human neutrophil immunodeficiency syndrome is associated with an inhibitory Rac2 mutation [J].
Ambruso, DR ;
Knall, C ;
Abell, AN ;
Panepinto, J ;
Kurkchubasche, A ;
Thurman, G ;
Gonzalez-Aller, C ;
Hiester, A ;
deBoer, M ;
Harbeck, RJ ;
Oyer, R ;
Johnson, GL ;
Roos, D .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2000, 97 (09) :4654-4659
[3]   OXYGEN-DEPENDENT MICROBIAL KILLING BY PHAGOCYTES .1. [J].
BABIOR, BM .
NEW ENGLAND JOURNAL OF MEDICINE, 1978, 298 (12) :659-668
[4]   The effect of hyperoxia on the expression of cytokine mRNA in endothelial cells. [J].
Darrington, RS ;
Godden, DJ ;
Park, MS ;
Ralston, SH ;
Wallace, HM .
BIOCHEMICAL SOCIETY TRANSACTIONS, 1997, 25 (02) :S292-S292
[5]   HYPEROXIA STIMULATES INTERLEUKIN-8 RELEASE FROM ALVEOLAR MACROPHAGES AND U937 CELLS - ATTENUATION BY DEXAMETHASONE [J].
DEATON, PR ;
MCKELLAR, CT ;
CULBRETH, R ;
VEAL, CF ;
COOPER, JAD .
AMERICAN JOURNAL OF PHYSIOLOGY, 1994, 267 (02) :L187-L192
[6]   THE SURGICAL IMPLICATIONS OF CHRONIC GRANULOMATOUS-DISEASE [J].
ECKERT, JW ;
ABRAMSON, SL ;
STARKE, J ;
BRANDT, ML .
AMERICAN JOURNAL OF SURGERY, 1995, 169 (03) :320-323
[7]   DIRECTLY MEASURED TISSUE OXYGEN-TENSION AND ARTERIAL OXYGEN-TENSION ASSESS TISSUE PERFUSION [J].
GOTTRUP, F ;
FIRMIN, R ;
RABKIN, J ;
HALLIDAY, BJ ;
HUNT, TK .
CRITICAL CARE MEDICINE, 1987, 15 (11) :1030-1036
[8]   Supplemental perioperative oxygen to reduce the incidence of surgical-wound infection [J].
Greif, R ;
Akça, O ;
Horn, EP ;
Kurz, A ;
Sessler, DI .
NEW ENGLAND JOURNAL OF MEDICINE, 2000, 342 (03) :161-167
[9]  
HARTMANN M, 1992, EUR J SURG, V158, P521
[10]  
Hopf H., 1996, WOUND REPAIR REGEN, V4, pA129