Boyd R. Endecott

Lack of an effect of interference with amine mechanisms on the lethality of chlordimeform in the rat.

Abstract Neither blockade of serotonergic nor α-adrenergic receptors (or both) nor depletion of tissue stores of these amines reduced the lethality in male rats of chlordimeform, an MAO-inhibiting insecticide which causes signs of sympathetic or serotonergic stimulation.

A study of the measurement of cholinesterase by constant-pH titration: the effect of hemolysins and a comparison with the electrometric technique.

Abstract Estimates of the degree of inhibition of cholinesterase activity in samples of blood from human beings by 1-naphthyl N-methylcarbamate (carbaryl, Sevin) and by diethylparanitrophenylphosphate (paraoxon) are higher by constant-pH titration than by the electrometric method of Michel. The hemolysin, alkyl phenoxy polyethoxy ethanol (Triton X-100), 0.2%, inhibits approximately 70% of the acetylcholine-hydrolyzing ability of blood plasma and therefore results in low estimates of acetylcholinesterase when used with whole blood and with plasma, if acetylcholine is used as the substrate.

The Effect of Elevated Temperature on Carbon Monoxide-Induced Incapacitation

Laboratory rats were exposed to experimental concentrations of carbon monoxide in air at ambient temperature, to elevated temperature at mospheres from 40°C to 60°C, and to selected CO concentrations in 40-60°C whole-body environments. Incapacitating potency was evaluated by measuring time-to-incapacitation as a function of CO concentration and/or temperature. Incapacitation occurred earlier when CO inhalation was combined with elevated temperature than when the same parameters were applied individ ually ; a fractionally additive effect was noted. An empirical equation was derived for predicting time-to-incapacitation from CO concentration and tem perature data.

Depression of cholinesterase activity by ethylestrenol in organophosphorus-poisoned and normal rats

Abstract The twice-daily oral administration of ethylestrenol to nonpoisoned rats depressed cholinesterase activity in the brain, stomach, and diaphragm. In rats chronically poisoned with disulfoton, ethylestrenol reduced the rate of return of cholinesterase activity in the stomach and diaphragm but not in the brain. Ethylestrenol also decreased the rate of weight gain of both poisoned and nonpoisoned animals.