[Therapy for poisonings--antidote. 3. Antidote indications B-E].
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[Therapy for poisonings--antidotes. 4. Antidote indications F-K].
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Antidotes↗
[Therapy for poisonings antidotes. Antidote indications L-Z].
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[Therapy for poisonings--antidotes. 1. The ABC of poisoning treatment, antidotes (indications, dosage)].
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Antidotes↗
The efficiency of aquocobalamine as an antidote in cyanide poisoning when given alone or combined with sodium thiosulfate.
The antidotal activities of aquocobalamineacetates and sodium thiosulfate were tested in guinea pigs and cats. The animals were attached to artificial respirators throughout the experiment and were poisoned with a continuous infusion of sodium cyanide solution (4.1 muMol/kg.min NaCN). The rate of action of each antidote was determined from the time taken for the HCN exhalation to drop below the level of 100 nMol/kg.min in quinea pigs, and to values below 25 nMol/kg.min in cats; the detoxifying capacity of each antidote was determined from the time taken for the HCN exhalation to rise above the said values and the time interval for normal function of heart activity to be restored. Aquobalamine was characterized by its rapid rate of reaction in both the animal species; its detoxifying capacity showed, however, according to our expectations, variations corresponding to the applied doses. The combination of the antidotes aquocobalamine (100 mg/kg) and thiosulfate (500 mg/kg) proved to possess high rate of reaction and a large detoxifying capacity in guinea pigs. Similar results were obtained in cats with antidote doses of 200 mg/kg aquocobalamine combined with 500 mg/kg thiosulfate. The slow rate of reaction and large detoxifying capacity of thiosulfate were confirmed in our experiments. It combination with aquocobalamine showed no undesirable change in its antidotal action providing a time interval of 1 min was maintained between the 2 injections.
Animals↗
[Arsenic metabolism. (17) Studies of placental transfer of arsenic and the effects of antidotes and diet].
Albino rats of Wistar strain (Tamura 1950) breeded in a closed colony were administered arsenic trioxide orally during pregnancy (from the 0 day to the 20th day). Organs of fetuses and mother rats were exenterated on the 21st day of gestation and the contents of arsenic measured using an arsenic analyzer unit with atomic absorption spectrophotometry. Whole organs of the fetus were separated into 3 groupings i.e. liver, brain and remaining organs. The contents of arsenic in the organs in each of these groupings and in the placenta were measured. Even in the non-administered group, arsenic was detected in the every organ. In the arsenic administered group, the content of arsenic in the placenta was the highest among the four preparations tested; and the content in the liver and remaining organs was considerably high, but was low in the brain. The level of accumulation of arsenic differed between each organ. In the placenta, the accumulation reached a plateau, and in the brain this accumulation was below one-tenth that in the liver. In the non-administered group, arsenic was detected in the liver, kidney, spleen and brain of mother rats. In the group on arsenite, the content in the kidney and spleen was large, followed by a large amount in the liver and in the brain respectively. The level of accumulation of arsenic in mother rats differed between each organ. Arsenite was administered with antidotes such as dimercaprol, thioctic acid and L-ascorbic acid during pregnancy (from the 0 day to the 5th day). In this group the content of arsenic in the remaining organs was statistically less than that of the control group. The content in the brain was slightly reduced by a co-administration of the antidotes, however, there was no statistical difference in the placenta and liver between the antidote-treated and control groups. The content of arsenic in the kidney of mother rats treated with antidotes was statistically less than that of the controls. Whether or not the content of arsenic in organs of fetuses and mother rats was affected by a milk diet was also studied. The content of arsenic in the organs of fetuses showed no statistical difference between the animals on an Oriental stock diet group and those on the milk diet. On the other hand, the content of arsenic in the kidney of mother rats on the milk diet was statistically less than seen in those in the Oriental stock diet group.
Animals↗
Antidote effect of liquid paraffin in oral solvent intoxication.
The antidote efficacy of liquid paraffin in oral solvent intoxications was investigated in dogs. Groups of 3 to 4 animals each received 1 ml/kg of methylchloroform, 0.3 ml/kg of benzene, or 3 ml/kg of a synthetic gasoline mixture (hexane/heptane/octane, ratio 30:50:20) by gastric intubation. After a prolonged interval the same animals were given 5 ml/kg of liquid paraffin by a separate tube in addition to one of the above solvents. The solvent concentrations in the blood were determined by gas chromatography at appropriate intervals. Administration of liquid paraffin in conjunction with methylchloroform does not significantly affect the absorption process. In the case of benzene and the synthetic gasoline mixture, however, liquid paraffin produces a distinct reduction in the rate of absorption. It is thus concluded that in the therapy of oral solvent-intoxication, liquid paraffin exhibits favorable antidote properties which may however differ from one solvent to the other. In clinically relevant situations involving coadministration of purgatives, the antidote effect must be assessed as being of a higher order than in our animal experiments in which purgatives had to be omitted for external reasons.
Animals↗
The in vivo effects of cyanide and its antidotes on rat brain cytochrome oxidase activity.
The in vivo effects of sodium cyanide and its antidotes, sodium nitrite, sodium thiosulfate and 4-dimethylaminophenol (DMAP), as well as the alpha-adrenergic blocking agent phentolamine, on rat brain cytochrome oxidase were studied. The course of inhibition was time-dependent and a peak of 40% was attained between 15 and 20 min after the s.c. injection of 1.3 LD50 (12 mg/kg) of cyanide. Pronounced dose-dependence was observed in the inhibition of the enzyme, at this relatively low, but lethal dose. Further observation was impossible because of rapidly lethal effects of cyanide. In animals artificially ventilated with room air, observation was possible up to 60 min. However, maximum inhibition was also 40%. When antidotes were applied 30 min after 20 mg/kg of cyanide, marked reactivation of cytochrome oxidase activity was observed with all antidotes (particularly with thiosulfate) except for phentolamine which had no effect. Prevention of methemoglobin forming with toluidine blue did not affect the reactivating ability of nitrite or DMAP, thus suggesting more complex protective mechanisms then simple methemoglobin formation. The high efficacy of thiosulfate may be attributed to its rhodanese catalyzed, direct binding to free blood cyanide, leading thus to its dissociation from cytochrome oxidase. The theory that cytochrome oxidase inhibition is a basic mechanism of cyanide toxicity could not be disproved.
Aminophenols↗
Comparisons of antidotal efficacy of chelating drugs upon acute toxicity of Ni(II) in rats.
Six chelating drugs were administered to rats by im injection at equimolar dosages in order to compare their relative effectiveness in prevention of death after a single parenteral injection of NiCl2. Triethylenetetramine and d-penicillamine were most effective antidotes for acute Ni (II)-toxicity. In order of decreasing antidotal effectiveness, diglycyl-L-histidine-N-methylamide, sodium diethyldithiocarbamate and calcium disodium versenate significantly reduced the acute mortality of rats following ip injection of Ni (II). Alpha-Lipoic acid was not effective as an antidote for acute Ni (II)-toxicity.
Animals↗
[Effect of antidotes on the rate of absorption of 2,4-dinitrophenol from the digestive tract into the blood].
An investigation of the rate of the 2,4-dinitrophenol absorption from the digestive tract into the blood with the use of an antidote and its components (activated charcoal, tannin, magnesium oxide), stach water and paraffin oil demonstrated the activated charcoal and magnesium oxide to be the best antidotes among the ones studied. The antidote exerts a somewhat less marked, but still quite a strong action.
Animals↗
Efficacy of pralidoxime iodide and obidoxime dichloride as antidotes in diazinon-poisoned goslings.
The antidotal efficacy of pralidoxime iodide and obidoxime dichloride was investigated in goslings poisoned by a supralethal dose of the organophosphorus insecticide diazinon. Various doses of both drugs were administered by intramuscular injection when the poisoned birds were unable to walk. Pralidoxime at 100 mg/kg brought about a complete and speedy clinical recovery. Fifty mg/kg induced recovery in 4 of 6 poisoned goslings, and 25 mg/kg successfully trated only 1 of 6 birds. Obidoxime at 25 mg/kg showed no therapeutic properties whereas 50 and 100 mg/kg delayed the death of some birds by several hours. At 100 mg/kg, all goslings had transient signs of intoxication, which precluded the use of this compound as an antidote at higher doses. The mode of action of these antidotes in diazinon-poisoned goslings is discussed.
Animals↗
Interference by tannic acid with the effectiveness of activated charcoal in "universal antidote".
Evidence is presented to show that tannic acid is responsible for the reduced effectiveness of "universal antidote" as compared with activated charcoal alone. Adsorption isotherm data indicate that tannic acid binds strongly to charcoal and hence uses up part of the adsorption capacity that would otherwise be available for binding of a drug or poison. Data on sodium salicylate adsorption from simulated gastric fluid, both with and without the presence of tannic acid, are presented that illustrate clearly that tannic acid interferes significantly with the adsorption of salicylate. Magnesium oxide, another component of "universal antidote," was found to offer no interference to salicylate adsorption, presumably because it does not adsorb to charcoal to any significant extent.
Adsorption↗
Antidotal therapy and changes of acetylcholinesterase activity following isopropyl methylphosphonofluoridate intoxication in mice.
The antidotal action of atropine with trimedoxime, obidoxime or methoxime against isopropyl methylphosphonofluoridate intoxication in mice was studied. The best antidotal effect was demonstrated for the combination of atropine and methoxime (tested as therapeutic index or D50 index). The effect of atropine (constant dose) and methoxime (different doses) on acetylcholinesterase (AChE) activity in four parts of the mouse brain following isopropyl methylphosphonofluoridate intoxication was described. The therapeutic effect could be improved by increasing dose of methoxime. AChE activity in the pontomedullar area was increased on increasing the dose of methoxime (p less than 0.005). A correlation between residual AChE activity in the pontomedullar part of the mouse brain and mortality was demonstrated.
Acetylcholinesterase↗
Comparisons of antidotal efficacy of sodium diethyldithiocarbamate, D-penicillamine and triethylenetetramine upon acute toxicity of nickel carbonyl in rats.
Sodium diethyldithiocarbamate, D-penicillamine, and triethylene-tetramine were administered to rats by im injection in dosages equivalent to 0.6 times their respective LD50 values in order to compare their relative effectiveness in prevention of death caused by exposure for 15 min to inhalation of nickel carbonyl (1.4 or 4.2 mg Ni (CO)4/liter of air). When the three drugs were administered to groups of rats at 10 min before or after the exposure to nickel carbonyl, sodium diethyldithiocarbamate was the most effective antidote. In contrast, then the drugs were administered at 6 hr after exposure to nickel carbonyl, D-penicillamine was the most effective antidote. Based upon the combined results of 4 sets of experiments, sodium diethyldithiocarbamate and D-penicillamine were significantly more effective than triethylenetetramine. The authors recommend that sodium diethyldithio-carbamate should remain the chelating agent of choice for therapy of nickel carbonyl poisoning. If sodium diethyldithiocarbamate is not available or if its use is contraindicated, D-penicillamine might be considered as an alternative chelating agent.
Animals↗
[Electrophysiologic shifts in the functional antagonism between phosphororganic pesticides and their antidotes].
The authors carried out studies on 18 nonanesthetised and anesthetised cats under the conditions of complete imobilization with tricuran and under artificial respiration and examined the temporary consequence of the effects on the spontaneous and induced cerebral activity after poisoning with lethal doses of phosdrine and treatment with Doline, which is the therapeutic antidote of phosphorganic pesticides. The authors established that after lethal poisoning with phosdrin the secondary induced cerebral hypoxia enhanced deepening of the disintegration in the intercerebral interrelationships, which caused the appearence of epileptiform activity. The antidote Doline within 1-2 minutes, after its muscular administration abolished effectively the generalized epileptic seizure and repaired quickly the electrophysiological indices-peculiar for the normal EEG.
Animals↗
Sugar-oximes, new potential antidotes against organophosphorus poisoning.
In attempt to improve distribution and transport qualities of antidotes against organophosphorus poisoning, a new series of pyridine aldoximes linked to glucose moiety were synthesized and studied both in vivo and in vitro. Preliminary results describing the biological activity of the new compounds are presented and discussed in this report.
Animals↗
Effect of cyanide antidotes on the metabolic conversion of cyanide to thiocyanate.
The excretion of thiocyanate following the administration of equitoxic doses of cyanide to unprotected mice and to animals pretreated with various cyanide antidotes has been studied. The results demonstrate that cyanide given alone or to animals pretreated with thiosulfate is extensively converted to thiocyanate. Animals pretreated with sodium nitrite or a combination of nitrite and sodium thiosulfate excreted even higher amounts of thiocyanate. This demonstrates that cyanide originally detoxified by combination with methemoglobin is ultimately converted to thiocyanate in the animal body. Pretreatment of animals with cobalt compounds (cobaltous chloride or dicobalt-EDTA) or a combination of cobalt compounds and thiosulfate resulted, on the other hand, in a less efficient conversion of cyanide to thiocyanate. The cyanide detoxified by trapping as highly undissociated cobalt-cyanide complexes is instead excreted in the urine, as demonstrated by detection of high amounts of cobalt ions and strongly complex-bound cyanide in the urine from animals treated with cobalt compounds and cyanide. A method for the determination of cyanide present as cobalt-cyanide complexes is described and its forensic application is proposed.
Animals↗
A "superactive" charcoal for antidotal use in poisonings.
Amoco Grade PX-21 powdered activated charcoal was found to adsorb nearly three times as much sodium salicylate from simulated gastric fluid than did another charcoal (Norit A), which is representative of the best of all other charcoals heretofore available. This indicates the potential superior effectiveness of the Amoco charcoal as an oral antidote in poisonings.
Adsorption↗