Matchett Gerald A, Martin Robert D, Zhang John H
Department of Anesthesiology, Loma Linda University School of Medicine, Loma Linda, CA 92350, USA.
Neurol Res. 2009 Mar;31(2):114-21. doi: 10.1179/174313209X389857.
Numerous studies have demonstrated a protective effect of hyperbaric oxygen therapy in experimental ischemic brain injury, and many physiological and molecular mechanisms of hyperbaric oxygen therapy-related neuroprotection have been identified.
Review of articles pertaining to hyperbaric oxygen therapy and cerebral ischemia in the National Library of Medicine and National Institutes of Health database, emphasizing mechanisms of hyperbaric oxygen therapy-related neuroprotection.
Hyperbaric oxygen therapy has been shown to ameliorate brain injury in a variety of animal models including focal cerebral ischemia, global cerebral ischemia, neonatal hypoxia-ischemia and subarachnoid hemorrhage. Small human trials of hyperbaric oxygen therapy in focal ischemia have not shown benefit, although one trial of hyperbaric oxygen therapy before cardiopulmonary bypass demonstrated improved neuropsychological and inflammatory outcomes with hyperbaric oxygen therapy. Hyperbaric oxygen therapy is associated with improved cerebral oxygenation, reduced blood-brain barrier breakdown, decreased inflammation, reduced cerebral edema, decreased intracranial pressure, reduced oxidative burden, reduced metabolic derangement, decreased apoptotic cell death and increased neural regeneration.
On a molecular level, hyperbaric oxygen therapy leads to activation of ion channels, inhibition of hypoxia inducible factor-1alpha, up-regulation of Bcl-2, inhibition of MMP-9, decreased cyclooxygenase-2 activity, decreased myeloperoxidase activity, up-regulation of superoxide dismutase and inhibition of Nogo-A (an endogenous growth-inhibitory factor). Ongoing research will continue to describe the mechanisms of hyperbaric oxygen therapy-related neuroprotection, and possibly expand hyperbaric oxygen therapy use clinically.
大量研究已证明高压氧疗法对实验性缺血性脑损伤具有保护作用，并且已经确定了许多与高压氧疗法相关的神经保护的生理和分子机制。
回顾美国国立医学图书馆和国立卫生研究院数据库中有关高压氧疗法和脑缺血的文章，重点关注与高压氧疗法相关的神经保护机制。
高压氧疗法已被证明可改善多种动物模型中的脑损伤，包括局灶性脑缺血、全脑缺血、新生儿缺氧缺血和蛛网膜下腔出血。尽管一项在体外循环前进行高压氧疗法的试验表明高压氧疗法可改善神经心理和炎症结局，但在局灶性缺血中进行的小型人体高压氧疗法试验未显示出益处。高压氧疗法与改善脑氧合、减少血脑屏障破坏、减轻炎症、减轻脑水肿、降低颅内压、减轻氧化负担、减少代谢紊乱、减少凋亡细胞死亡以及增加神经再生有关。
在分子水平上，高压氧疗法可导致离子通道激活、缺氧诱导因子-1α抑制、Bcl-2上调、MMP-9抑制、环氧合酶-2活性降低、髓过氧化物酶活性降低、超氧化物歧化酶上调以及Nogo-A（一种内源性生长抑制因子）抑制。正在进行的研究将继续描述与高压氧疗法相关的神经保护机制，并可能在临床上扩大高压氧疗法的应用。
