Mink R B, Dutka A J
National Naval Medical Center, Naval Medical Research Institute, Bethesda, MD, USA.
Crit Care Med. 1995 Aug;23(8):1398-404. doi: 10.1097/00003246-199508000-00014.
To determine whether hyperbaric oxygen administered immediately after global cerebral ischemia increases free radical generation and lipid peroxidation in the brain or alters neurophysiologic recovery.
Prospective, randomized, controlled trial.
Animal research laboratory.
Adult male New Zealand white rabbits.
Anesthetized rabbits were subjected to 10 mins of global cerebral ischemia by infusing a mock cerebrospinal fluid into the subarachnoid space and increasing intracranial pressure equal to mean arterial pressure. Immediately upon reperfusion, one group of rabbits (n = 9) was treated with hyperbaric oxygen at 2.8 atmospheres absolute for 75 mins while the control group (n = 9) breathed room air for an equivalent period of time. At the end of the reperfusion period, oxyradical brain damage was determined by measuring brain levels of oxidized and total glutathione and free malondialdehyde. Neurophysiologic brain injury was assessed with cortical somatosensory evoked potentials.
Both oxidized glutathione and the ratio of oxidized glutathione to reduced glutathione (total minus oxidized) were higher (p < .05) in the hyperbaric oxygen group, indicating that hyperbaric oxygen increased free radical generation. Nonetheless, brain malondialdehyde content, an index of lipid peroxidation, was similar (p > .05) in the two groups. Cortical somatosensory evoked potential recovery at the end of reperfusion was 50% higher (p < .05) in the hyperbaric oxygen-treated animals compared with controls.
Treatment with hyperbaric oxygen after ischemia increased the amount of oxygen free radicals in the brain. However, this increase in free radical generation was not associated with an increase in lipid peroxidation or a reduction in neurophysiologic recovery when measured after 75 mins of recirculation. These results suggest that hyperbaric oxygen administered immediately after global ischemia does not promote early brain injury.
确定全脑缺血后立即给予高压氧是否会增加脑内自由基生成和脂质过氧化，或改变神经生理恢复情况。
前瞻性、随机、对照试验。
动物研究实验室。
成年雄性新西兰白兔。
通过向蛛网膜下腔注入模拟脑脊液并将颅内压升高至平均动脉压，使麻醉后的兔子经历10分钟的全脑缺血。再灌注即刻，一组兔子（n = 9）接受2.8个绝对大气压的高压氧治疗75分钟，而对照组（n = 9）在相同时间段内呼吸室内空气。在再灌注期结束时，通过测量脑内氧化型谷胱甘肽、总谷胱甘肽和游离丙二醛的水平来确定氧自由基脑损伤。用皮质体感诱发电位评估神经生理性脑损伤。
高压氧组的氧化型谷胱甘肽以及氧化型谷胱甘肽与还原型谷胱甘肽（总量减去氧化型）的比值均较高（p < 0.05），表明高压氧增加了自由基生成。尽管如此，两组的脑丙二醛含量（脂质过氧化指标）相似（p > 0.05）。与对照组相比，高压氧治疗的动物在再灌注结束时皮质体感诱发电位的恢复高50%（p < 0.05）。
缺血后给予高压氧治疗增加了脑内氧自由基的量。然而，在再循环75分钟后测量时，这种自由基生成的增加与脂质过氧化的增加或神经生理恢复的降低无关。这些结果表明，全脑缺血后立即给予高压氧不会促进早期脑损伤。
