Al-Waili Noori S, Butler Glenn J
Life Support Technologies, Inc., Chronic Wound Treatment and Hyperbaric Medicine Center, The Mount Vernon Hospital, Mount Vernon, NY 10550, USA.
ScientificWorldJournal. 2006 Apr 3;6:425-41. doi: 10.1100/tsw.2006.78.
There is growing interest in expanding the clinical applications for HBO2 (hyperbaric oxygen therapy) into new medical and surgical fields. The pathophysiology of response towards wounds, infection, trauma, or surgery involves various chemical mediators that include cytokines, prostaglandins (PGs), and nitric oxide (NO). The beneficial role played by HBO2 in wound healing, carbon monoxide poisoning, decompression sickness, and other indications is well documented. However, the exact mechanism of action is still poorly understood. This review addresses the effects of HBO2 on PGs, NO, and cytokines involved in wound pathophysiology and inflammation in particular. The results of this review indicate that HBO2 has important effects on the biology of cytokines and other mediators of inflammation. HBO2 causes cytokine down-regulation and growth factor up-regulation. HBO2 transiently suppresses stimulus-induced proinflammatory cytokine production and affects the liberation of TNFa (tumor necrosis factor alpha) and endothelins. VEGF (vascular endothelial growth factor) levels are significantly increased with HBO2, whereas the value of PGE2 and COX-2 mRNA are markedly reduced. The effect of HBO2 on NO production is not well established and more studies are required. In conclusion, cytokines, PGs, and NO may play a major role in the mechanism of action of HBO2 and further research could pave the way for new clinical applications for HBO2 to be established. It could be proposed that chronic wounds persist due to an uncontrolled pathological inflammatory response in the wound bed and that HBO2 enhances wound healing by damping pathological inflammation (anti-inflammatory effects); this hypothetical proposal remains to be substantiated with experimental results.
将高压氧疗法（HBO2）的临床应用扩展到新的医学和外科领域的兴趣日益浓厚。对伤口、感染、创伤或手术的反应的病理生理学涉及多种化学介质，包括细胞因子、前列腺素（PGs）和一氧化氮（NO）。HBO2在伤口愈合、一氧化碳中毒、减压病和其他适应症中所起的有益作用已有充分记录。然而，其确切的作用机制仍知之甚少。本综述特别探讨了HBO2对参与伤口病理生理学和炎症的PGs、NO和细胞因子的影响。本综述结果表明，HBO2对细胞因子和其他炎症介质的生物学有重要影响。HBO2导致细胞因子下调和生长因子上调。HBO2可短暂抑制刺激诱导的促炎细胞因子产生，并影响肿瘤坏死因子α（TNFα）和内皮素的释放。HBO2可使血管内皮生长因子（VEGF）水平显著升高，而前列腺素E2（PGE2）和环氧化酶-2（COX-2）mRNA的值则明显降低。HBO2对NO产生的影响尚未明确，需要更多研究。总之，细胞因子、PGs和NO可能在HBO2的作用机制中起主要作用，进一步的研究可为建立HBO2的新临床应用铺平道路。可以提出，慢性伤口持续存在是由于伤口床中不受控制的病理性炎症反应，而HBO2通过抑制病理性炎症（抗炎作用）促进伤口愈合；这一假设仍有待实验结果证实。
