Latent dichlorvos neurotoxicity detected by vagal tone monitoring in dogs.
Dichlorvos (dimethyl 2,2-dichlorovinyl phosphate) was administered orally to German Shorthair Pointer dogs at approximately 60 mg/kg (twice the usual clinical dose). Plasma and erythrocyte cholinesterase (ChE) was monitored prior to, 90 min, and 180 min post-ingestion. 2-PAM (20 mg/kg IV) and atropine sulfate (0.022 mg/kg IM) were administered 90 min after the dichlorvos to paired treated and control dogs. The telemetered electrocardiographic (ECG) signal was analyzed by a Vagal Tone Monitor (VTM) to yield mean heart period (msec) and an estimate of the amplitude of respiratory sinus arrhythmia (V in natural log values of msec2) for five min intervals. Dichlorvos did not cause cholinomimetic symptoms even though blood cholinesterase was significantly inhibited (plasma -51.3% and erythrocyte -43.7%). The atropine sulfate treatment resulted in the expected vagolytic effects in both the control and the dichlorvos treated dogs, but the atropine effects were attenuated in the latter dogs. Three weeks later, ChE activity was not significantly depressed in the dichlorvos treated dogs, and their V responses to atropine were more similar to the responses in control dogs.
D000818:Animals; D001285:Atropine / Q000627:therapeutic use; D002802:Cholinesterases / Q000097:blood; D004006:Dichlorvos / Q000037:antagonists & inhibitors / Q000633:toxicity*; D004285:Dogs; D004912:Erythrocytes / Q000201:enzymology; D008991:Monitoring, Physiologic; D009422:Nervous System Diseases / Q000139:chemically induced* / Q000503:physiopathology; D011220:Pralidoxime Compounds / Q000627:therapeutic use; D014630:Vagus Nerve / Q000503:physiopathology*
D011220:Pralidoxime Compounds; D001285:Atropine; D004006:Dichlorvos; D002802:Cholinesterases