Ischaemia-reperfusion injury of the peripheral nerve: An experimental study

Citation
A. Saray et al., Ischaemia-reperfusion injury of the peripheral nerve: An experimental study, MICROSURG, 19(8), 1999, pp. 374-380
Citations number
28
Categorie Soggetti
Surgery
Journal title
MICROSURGERY
ISSN journal
07381085 → ACNP
Volume
19
Issue
8
Year of publication
1999
Pages
374 - 380
Database
ISI
SICI code
0738-1085(1999)19:8<374:IIOTPN>2.0.ZU;2-3
Abstract
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.