(HOME) 
Subject: peripheral neuropathy

   
   Ann Plast Surg 1998 Feb;40(2):156-9
   
Role of reactive oxygen species in optic nerve compression injury: a
preliminary study.

    Babovic S, Im MJ, Angel MF, Manson PN
    
   Division of Plastic, Reconstructive and Maxillofacial Surgery, The
   Johns Hopkins University School of Medicine, Baltimore, MD, USA.
   
   Optic nerve compression is one of the complications in craniofacial
   surgery and blepharoplasty. We have shown previously that acute and
   chronic nerve compression produce significant tissue injury in rat
   sciatic nerve. In the present study the optic nerve was evaluated for
   possible ischemia/reperfusion injury after acute compression in an
   animal model. Male New Zealand White rabbits were used in the
   experiment. The optic nerve was subjected to 2-hour compression
   followed by reperfusion for 1 hour. Nerve compression was established
   by banding the optic nerve with silastic tubing. The compressed optic
   nerve was assayed for malondialdehyde, an indicator of lipid
   peroxidation, measured as thiobarbituric acid reactive substances
   (TBARS). The TBARS levels increased significantly to 2.5 times normal,
   from 37+/-6 pmoles per milligram tissue (N=6) to 90+/-12 pmoles per
   milligram tissue dry weight (N=5) in the compressed/reperfused nerve
   (p < 0.05). Much of these increases were prevented by treatment with
   deferoxamine, an iron chelator and antioxidant. The results indicate
   that optic nerve is injured by acute compression followed by
   reperfusion. The nerve compression injury appears to be due to
   reactive oxygen species and can be ameliorated by treatment with free
   radical scavengers.
   
   PMID: 9495464, UI: 98154852
     _________________________________________________________________
   
 ________________________________________________________________

(HOME)