Although the neuropathology of ischaemic fibre degeneration is relatively w
ell known, its pathogenesis is poorly understood. One of the presumed mecha
nisms is oxidative stress, causing the breakdown of the blood-nerve barrier
(BNB) and ending in lipid peroxidation, We evaluated the effect of ischaem
ia and reperfusion on the sciatic-tibial nerve of the rat and investigated
the biochemical, pathological, and functional evidence of BNB disruption an
d lipid peroxidation. The distal portion and trifurcation of the sciatic ne
rve were rendered ischaemic by clamping the femoral vessels for 3 h and fol
lowed by varying durations of reperfusion. Reperfusion resulted in an incre
ase in lipid peroxidation beginning from the first hour and increasing unti
l the seventh day, followed by a gradual decline over the following weeks,
Nerve oedema and ischaemic fibre degeneration (IFD) consistently became mor
e severe and prominent with reperfusion, indicating that oxidative stress d
amages the BNB and causes IFD, Results of functional testing by the sciatic
function index correlated with other parameters as walking track analysis
results got worse as reperfusion periods increased. impairment of walking p
atterns was more striking after the first day and continued up to the third
week, These data indicate that severe ischaemia of the peripheral nerve re
sults in reperfusion injury, functional impairment, and disruption of the B
NB, Microvascular events, which may occur during reperfusion, may be import
ant in amplifying the nerve fibre degeneration that initiated during ischae
mia, (C) 1999 Wiley-Liss, Inc.