ISCHEMIC REPERFUSION CAUSES LIPID-PEROXIDATION AND FIBER DEGENERATION

Although the neuropathology of ischemic fiber degeneration (IFD) is re latively well known, its pathogenesis is poorly understood. One putati ve mechanism of IFD is oxidative stress, causing a breakdown of the bl ood-nerve barrier (BNB) and lipid peroxidation, We evaluated the effec t of ischemic reperfusion of rat sciatic-tibial nerve seeking biochemi cal 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. Reperfu sion resulted in an increase in nerve lipid hydroperoxides, greatest a t 3 h, followed by a gradual decline over the next month. Nerve edema and IFD consistently became more severe with reperfusion, indicating t hat oxidative stress impairs the BNB (edema) and causes IFD, Reduced r eperfusion was greatest over distal sciatic nerve and midtibial nerve at day 7. The most ischemic segment (midtibial), of nonreperfused isch emic nerves (duration 3 h), underwent both edema and IFD that was as p ronounced as those of other segments after reperfusion, and underwent a smaller increase with reperfusion, suggesting that ischemia alone ca n also cause IFD and edema. The type of fiber degeneration was that of axonal degeneration. (C) 1996 John Wiley & Sons, Inc.