The role of nitric oxide in the neuropathology in soman intoxication.

Abstract:

:Intoxication with organophosphorus (0P) anticholinesterase agents such as soman triggers irreversible lesions in some cerebral areas. Administration of soman at the LD 50 leads to an increased activity of NADPH-diaphorase (= NO-synthase) in the cerebral endothelial cells from the 6th hour after poisoning. This activity culminates after 24 h, whereas variations in this enzymatic activity are not easily detectable in NADPH-diaphorase positive neurons. Since soman triggers astrocytic oedema leading to a possible decrease in the local cerebral blood flow, it is likely that the induction of endothelial NO-synthase exerts an antagonistic effect, since NO is a vasodilator.

journal_name

Brain Res

journal_title

Brain research

authors

Bouchaud C,Chollat-Namy A,Duserre S,Delamanche IS

doi

10.1016/0006-8993(94)91296-3

subject

Has Abstract

pub_date

1994-10-17 00:00:00

pages

249-54

issue

2

eissn

0006-8993

issn

1872-6240

pii

0006-8993(94)91296-3

journal_volume

660

pub_type

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