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

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.