Nagamatsu M, Schmelzer J D, Zollman P J, Smithson I L, Nickander K K, Low P A
Department of Neurology, Mayo Foundation, Rochester, Minnesota 55905, USA.
Muscle Nerve. 1996 Jan;19(1):37-47. doi: 10.1002/mus.880190103.
Although the neuropathology of ischemic fiber degeneration (IFD) is relatively well known, its pathogenesis is poorly understood. One putative mechanism of IFD is oxidative stress, causing a breakdown of the blood-nerve barrier (BNB) and lipid peroxidation. We evaluated the effect of ischemic reperfusion of rat sciatic-tibial nerve seeking biochemical and pathologic evidence of BNB disruption and lipid peroxidation. Ischemia, caused by the ligation of the supplying arteries to sciatic-tibial nerve, was maintained for 3 h, followed by reperfusion. Reperfusion resulted in an increase in nerve lipid hydroperoxides, greatest at 3 h, followed by a gradual decline over the next month. Nerve edema and IFD consistently became more severe with reperfusion, indicating that oxidative stress impairs the BNB (edema) and causes IFD. Reduced reperfusion was greatest over distal sciatic nerve and midtibial nerve at day 7. The most ischemic segment (midtibial), of nonreperfused ischemic nerves (duration 3 h), underwent both edema and IFD that was as pronounced as those of other segments after reperfusion, and underwent a smaller increase with reperfusion, suggesting that ischemia alone can also cause IFD and edema. The type of fiber degeneration was that of axonal degeneration.
尽管缺血性纤维变性（IFD）的神经病理学相对为人熟知，但其发病机制却了解甚少。IFD的一种推测机制是氧化应激，它会导致血神经屏障（BNB）破坏和脂质过氧化。我们评估了大鼠坐骨-胫神经缺血再灌注的影响，以寻找BNB破坏和脂质过氧化的生化及病理学证据。通过结扎坐骨-胫神经的供血动脉造成缺血，持续3小时，随后进行再灌注。再灌注导致神经脂质氢过氧化物增加，在3小时时达到最高，随后在接下来的一个月逐渐下降。随着再灌注，神经水肿和IFD持续加重，表明氧化应激损害了BNB（水肿）并导致IFD。在第7天，坐骨神经远端和胫神经中部的再灌注减少最为明显。未再灌注的缺血神经（持续时间3小时）中最缺血的节段（胫神经中部）出现了水肿和IFD，其程度与再灌注后其他节段相当，且再灌注时增加幅度较小，这表明仅缺血也可导致IFD和水肿。纤维变性的类型为轴突变性。
