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Rhesus monkeys were intoxicated with methyl alcohol, using an initial dose of 2 gm/kg and subsequent doses were administered in order to maintain an attenuated and prolonged state of intoxication. Arterial blood samples were drawn for methyl alcohol, formate, PO2, PCO2, and pH, which were monitored periodically throughout the course of the experiment. With the use of these procedures monkeys developed metabolic acidosis with the accumulation of formic acid in the blood and a corresponding decrease in blood bicarbonate. These animals served as models, which allowed for ocular evaluation for early signs related to methyl alcohol poisoning. A mechanism to explain toxicity is proposed and discussed.
A previous report detailed the derivation and validation of an equation for calculating the Gibbs free energy of liquid-solid adsorption via high-performance liquid chromatography (HPLC). This study utilizes an improved form of that equation in conjunction with an in vitro model of solute adsorption to give an ordered listing of the antidotal activity of activated charcoal towards different drugs and other chemicals. The in vitro model consists of an activated charcoal column with a nominal particle diameter of 15 micron and a surface area of 447 x 10(4) cm2/g, together with a series of acetonitrile:water mobile phases at pH 3. A simple and efficient procedure was developed for ranking the solutes. First, each compound was run in an acetonitrile(ACN):water mobile phase chosen to give a convenient retention time and ideal chromatographic response. The capacity factor for this mobile phase was extrapolated to give a predicted capacity factor for a 35:65 (v/v) ACN:water mobile phase using an empirical equation developed from the exhaustive chromatography of four standard compounds (phenobarbital, strychnine, cyclohexanone, methyl ethyl ketone) in a variety of ACN:water mobile phases. In addition to the standards, 12 other compounds (glutethimide, chlordiazepoxide, quinine, brucine, d-propoxyphene, pentobarbital, methyprylon, methadone, meperidine, codeine, antipyrine, morphine) were evaluated. Based on these data, the Gibbs free energies of liquid-solid adsorption for these compounds were calculated and used to evaluate activated charcoal as a poison antidote for them. The results indicate that a rapid and accurate estimation of the utility of activated charcoal as an antidote for drugs and toxic substances can be obtained from a single chromatographic run of the test compound.
Neuromuscular transmission in the Chinese cobra Naja naja atra was not affected by its own toxin (cobrotoxin) at a concentration of as high as 100 microM, while in the frog a concentration of less than 0.1 microM cobrotoxin depressed the amplitude of the end-plate potential to less than 10% of its original value within 30 min or directly blocked the nerve-evoked muscle action potential. The lack of effect of cobrotoxin was also observed in the nerve-muscle preparations from a pit viper (Agkistrodon blomhoffii brevicaudus) and three species of non-poisonous snakes (Elaphe dione, Elaphe bimaculata and Elaphe rufodorsata). On the other hand, the snake preparations were sensitive to the blocking effect of D-tubocurarine and less sensitive to that of atropine, indicating that the nicotinic acetylcholine receptor is responsible for transmission between the nerve and the skeletal muscle of the snake. We suggest that the snake nicotinic cholinergic receptor lacks the cobrotoxin binding-site.
Poison ivy and oak urushiols or their components were compared with the respective esterified derivatives for efficacy in oral desensitization of Hartley guinea pigs sensitized to urushiols. The esterified derivatives produced a significantly greater degree of hyposensitization than did free urushiol counterparts. Suppression produced by esterified urushiols was of longer duration than that produced by free urushiols. Groups of sensitized guinea pigs were given high (100 mg/kg) or low (10 mg/kg) doses of a mixture of acetylated, saturated urushiol congeners over a 1-, 2-, or 3-week period. High doses produced a greater degree of hyposensitization regardless of the dosage schedule used. Low doses did not produce significant hyposensitization unless given over a shorter (1 week) schedule. Large single booster doses (33 mg/kg/week) of the acetate derivatives produced a rebound in responsiveness when given, 2 weeks following the last dose of the initial series, to animals hyposensitized with 10 mg/kg. No such rebound in sensitivity occurred in animals given a series of high initial doses.
The Communicable Disease Report number 84/52 has given a clear indication that Campylobacter infections are now the most significant reported causes of gastrointestinal infection. The figures given indicate approximately 22,000 Campylobacter infections in 1984 as opposed to approximately 14,000 Salmonella infections, with, more importantly, the trend increasing with regard to Campylobacter, and decreasing with regard to Salmonella infections. Campylobacter enteritis would now appear to be a major problem both in terms of human suffering and in its economic effects. It is reported, for example, that at least 80,000 working days may be lost in the United Kingdom per year. The fundamental problem raised by Campylobacter enteritis is whether we need to have a standardized definition of food poisoning accepted in law to allow central government and local authorities to manage in particular the problems related to Campylobacter enteritis. From information available, it appears that local authorities have differing interpretations as to the classification and subsequent management of Campylobacter enteritis. In order to control the identified trend in the increase of Campylobacter infections, the need for a clear and explicit definition is rapidly becoming essential.