Time course of electrophysiologic effects induced by DI‐n‐butyl‐2,2‐dichlorovinyl phosphate (DBCV) in the adult hen

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Abstract
Previous work in our laboratory indicated that di‐n‐butyl‐2,2‐dichlorovinyl phosphate (DBCV) produced electrophysiologic changes in hen peripheral nerve that coincided with the development of histopathologic changes and neurologic signs of peripheral neuropathy. The purpose of the present study was to follow the time course for the development of the electrophysiologic changes and to determine whether pretreat‐ment with the phosphinate analog of DBCV (DBCV‐P), a nonageable organophos‐phorus compound, prevented these effects. Although significant electrophysilogic deficits occurred in the tibial and sciatic nerve 24 h after DBCV treatment, the most marked changes coincided with the onset of clinical signs of organophosphorus‐induced delayed neuropathy (14–21 d). The sciatic and tibial nerves were equally susceptible to DBCV in producing deficits characterized by changes in the relative refractory period and an increased strength‐duration threshold. Pretreatment with DBCV‐P prevented the clinical signs and also attenuated the electrophysiologic deficits induced by DBCV treatment. These data suggest that electrophysiologic deficits occur before clinical signs of organophosphorus‐induced delayed neuropathy (OPIDN) and may be indicative of a link between neurotoxic esterase (NTE) inhibition and onset of overt clinical toxicity.