Kihara M, McManis P G, Schmelzer J D, Kihara Y, Low P A
Department of Neurology, Mayo Foundation, Rochester, MN 55905.
Ann Neurol. 1995 Jan;37(1):89-94. doi: 10.1002/ana.410370116.
Hyperbaric oxygenation is effective in augmenting the delivery of oxygen to tissue, but also causes oxidative stress. As part of our focus on improving peripheral nerve salvage from ischemic fiber degeneration, we evaluated whether hyperbaric oxygenation rescues peripheral nerve, rendered ischemic by microembolization, from ischemic fiber degeneration. The supplying arteries of rat sciatic nerve were embolized with microspheres of 14 microns diameter at moderate (2 x 10(6)) and high (5.6 x 10(6)) doses. Rats were randomized to receive hyperbaric oxygenation treatment (2.5 atm 100% oxygen for 2 hours/day for 7 days beginning within 30 minutes of ischemia), or room air. End points for the embolized limb were (1) behavioral scores (0-11 in increasing levels of limb function), (2) nerve action potential of sciatic-tibial nerve, (3) nerve blood flow, and (4) histological grade as percentage of fibers undergoing ischemic fiber degeneration (0 = < 5%; 1 = 5-25%; 2 = 26-50%; 3 = 51-75%; 4 = > 76%). Nerve blood flow and nerve action potential were uniformly absent and more than 90% of fibers had degenerated in both control and treatment groups receiving high doses. Control and treatment groups receiving moderate doses were well matched by level of ischemia (8.5 +/- 0.3 [N = 18] vs 7.7 +/- 0.4 ml/100 gm/min [N = 18], p > 0.05) but were significantly different by behavior score (5.6 +/- 0.7 vs 9.2 +/- 0.5 [N = 19], p < 0.001), nerve action potential (1.4 +/- 1.0 vs 3.9 +/- 0.5 [N = 6], p < 0.05), and histology (2.4 +/- 0.4 [N = 5] vs 0.8 +/- 0.5 [N = 4], p < 0.05). On single teased fiber evaluation, the predominant abnormality was E (axonal degeneration). We conclude that hyperbaric oxygenation will effectively rescue fibers from ischemic fiber degeneration, providing the ischemia is not extreme.
高压氧疗在增加组织氧输送方面是有效的,但也会引起氧化应激。作为我们致力于改善外周神经从缺血性纤维变性中挽救的一部分,我们评估了高压氧疗是否能挽救因微栓塞而缺血的外周神经免于缺血性纤维变性。用直径14微米的微球以中等剂量(2×10⁶)和高剂量(5.6×10⁶)栓塞大鼠坐骨神经的供应动脉。将大鼠随机分为接受高压氧疗组(2.5个大气压100%氧气,每天2小时,共7天,在缺血30分钟内开始)或空气组。栓塞肢体的终点指标为:(1)行为评分(肢体功能水平从0到11分递增),(2)坐骨-胫神经的神经动作电位,(3)神经血流,以及(4)组织学分级,即发生缺血性纤维变性的纤维百分比(0 = <5%;1 = 5 - 25%;2 = 26 - 50%;3 = 51 - 75%;4 = >76%)。接受高剂量的对照组和治疗组神经血流和神经动作电位均消失,且超过90%的纤维发生了变性。接受中等剂量的对照组和治疗组在缺血程度上匹配良好(8.5±0.3 [N = 18] 对 7.7±0.4 ml/100 gm/min [N = 18],p>0.05),但在行为评分(5.6±0.7对9.2±0.5 [N = 19],p<0.001)、神经动作电位(1.4±1.0对3.9±0.5 [N = 6],p<0.05)和组织学(2.4±0.4 [N = 5] 对 0.8±0.5 [N = 4],p<0.