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The role of nitric oxide in the neuropathology in soman intoxication
C Bouchaud1, A Chollat-Namy, S Duserre
1Institute of Neurosciences, URA 1488 CNRS, Université Pierre et Marie Curie, Paris, France.
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.