ABSTRACT
A modified method was compared with an original electrometric method for measurement of erythrocyte acetylcholinesterase (EChE) activity in sheep. The mean +/- SD (pH/30 min) of EChE activity of 8 sheep measured by the modified procedure (0.70 +/- 0.15) was not significantly different from that of the original method (0.64 +/- 0.12). The inherently low plasma cholinesterase activity of the sheep as measured by the 2 methods were also not significantly different from each other (0.09 +/- 0.04 vs 0.10 +/- 0.04). The coefficient of variation of the modified method in measuring EChE activity was 8%. The method was used to demonstrate in vitro inhibition of sheep EChE activity by the organophosphorus and carbamate insecticides dichlorvos and methomyl, respectively. The method could be well-suited for rapid measurement of EChE activity in sheep, especially in cases of organophosphate and possibly carbamate poisoning.
Subject(s)
Acetylcholinesterase/blood , Erythrocytes/enzymology , Animals , Cholinesterase Inhibitors/pharmacology , Dichlorvos/pharmacology , Dose-Response Relationship, Drug , Female , Male , Methomyl/pharmacology , SheepABSTRACT
Male mice were treated orally with the organophosphorus insecticides fenamiphos and dichlorvos at 10 and 150 mg/kg, respectively. The insecticides produced signs of toxicosis characteristic of cholinesterase inhibition, and induced death in all treated mice. Pretreatment of mice with diphenhydramine HCl (20 and 30 mg/kg, subcutaneously) 15 min before either insecticide significantly (P less than 0.05) reduced the incidence of toxic manifestations (excessive salivation, Straub tail, and whole body tremor), delayed the onset of death, and increased the percentage of survivors. Doses of diphenhydramine less than 20 mg/kg were not so effective. The data indicated a protective property of diphenhydramine against organophosphorus insecticide-induced toxicosis.
Subject(s)
Dichlorvos/toxicity , Diphenhydramine/pharmacology , Insecticides/toxicity , Organophosphorus Compounds/toxicity , Animals , Cholinesterase Inhibitors/toxicity , Drug Antagonism , Male , Mice , Salivation/drug effects , Tremor/prevention & controlABSTRACT
Intraperitoneal (ip) administration of xylazine (1-6 mg/kg) in male rats significantly increased urine flow over a 2-hr period in a dose-dependent manner, while urine osmolality was significantly decreased. Xylazine at 4.5 and 6 mg/kg significantly increased sodium excretion, whereas the 3 and 6 mg/kg doses of xylazine significantly increased potassium excretion. Yohimbine injected ip at 0.5 or 1 mg/kg 15 min before xylazine (6 mg/kg, ip) significantly decreased urine flow by 44% and 64% respectively. Yohimbine also prevented the increase in sodium and potassium excretion induced by xylazine. The data indicate that yohimbine is of value in controlling the diuretic effect of xylazine in rats.
Subject(s)
Diuresis/drug effects , Thiazines/pharmacology , Xylazine/pharmacology , Yohimbine/pharmacology , Animals , Male , Osmolar Concentration , Potassium/urine , Rats , Sodium/urineABSTRACT
Physostigmine (1.5 mg/kg, s.c.) and neostigmine (1.0 mg/kg, s.c.) injection into male mice produced signs of toxicosis characteristic of cholinesterase inhibition and evoked death in 95 and 94% of the animals respectively. Diphenhydramine injections (5-30 mg/kg, s.c.) 15 min before physostigmine or neostigmine significantly increased the latency period to onset of death and the percentage of survivors. Diphenhydramine injection (20 mg/kg, s.c.) between -30 and +2 min (but not at +5 and +10 min) relative to physostigmine prevented lethality in 100% of the animals. The data indicated that diphenhydramine which possesses anticholinergic effects protected mice against physostigmine- and neostigmine-induced toxicosis.
