Valeur et Mécanisme D'action de L'oxygénothérapie Dans le Traitement de L'intoxication Cyanhydrique

Paulet, G

doi:10.3109/13813455509145402

Cited by 12 publications

(3 citation statements)

References 9 publications

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“…Venous oxygen saturation is determined by oxygen uptake, arterial oxygen concentration, hemoglobin concentration, and cardiac output. If other factors remain constant, inhibition of peripheral oxygen uptake by cyanide will elevate venous oxygen saturation [11].…”

Section: Discussionmentioning

confidence: 99%

Long-Term Neuropsychiatric Sequelae in a Survivor of Cyanide Toxicity Patient With Arterialization

Alqahtani

Alyousef

AlWatban

et al. 2020

Cureus

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Cyanide is one of the most rapidly acting poisons and accounts for many suicidal and homicidal deaths. Some natural products such as silk and wool can release cyanide when burned. Most patients who survive cyanide poisoning experience neurological sequelae. This report describes the case of a healthy 45-year-old Yemeni woman who was present during the burning of furniture in a closed space in her home. Upon admission, she displayed signs of inhalational injury, a black discoloration around her mouth and nostrils, and a first-degree burn on the left side of her neck. She experienced neuropsychiatric sequelae of cyanide poisoning, with deficits evolving over three months. Even after three months of treatment and continuous follow-up, she still showed signs of mild cognitive memory impairment along with word-finding difficulties and focal dystonia of her right hand.Full neurological and cognitive assessments are crucial to determine the neuropsychiatric sequelae of acute cyanide toxicity. Magnetic resonance imaging (MRI) can show the extent and structure of lesions in cyanide-sensitive regions of the brain, but it is not always diagnostic. The arterialization of venous blood gases may serve as an early clue to the diagnosis of cyanide poisoning.

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Section: Discussionmentioning

confidence: 99%

Long-Term Neuropsychiatric Sequelae in a Survivor of Cyanide Toxicity Patient With Arterialization

Alqahtani

Alyousef

AlWatban

et al. 2020

Cureus

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“…287 Amyl nitrite also affords some protection through methemoglobin formation,70 but its value is limited by the fact that in man the inhalation of maximally tolerated doses produces only relatively low levels of methemoglobin. 314 p-Aminopropiophenone is even more effective than sodium nitrite in promoting the formation of methemoglobin 194 , 428 and has been shown to be an effective cyanide antidote. 35o However, methemoglobin formation is somewhat delayed with this compound, and for this reason, it is likely to be of more value as a prophylactic than a therapeutic agent.…”

Section: Cyanide Antidotesmentioning

confidence: 99%

Clinical pharmacology of systemic antidotes

Done

1961

Clin Pharma and Therapeutics

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“…The antidotal action of hydroxocobalamin against cyanide has been studied by Mushett, Kelly, Boxer & Rickards (1952), Mercker & Bastian (1959b), Delga, Mizoule, Veverka & Bon (1961), Delga, Mizoule & Veverka (1961) and Paulet, Bernard & Olivier (1963), and the compound was found to be effective. Various other cobalt complexes have also been tried, notably dicobalt edetate (the chelate of two cobalt atoms with ethylenediamine tetracetic acid), of cobalt with histidine, and also the gluconate and glutamate of cobalt (Paulet, 1957(Paulet, , 1958(Paulet, , 1960Mercker & Bastian, 1959a, b;Bartelheimer, 1962b;Tauberger & Klimmer, 1963). This paper describes a study and comparison of the antidotal actions of cobalt salts, hydroxocobalamin, the hydrolysis product cobinamide, and dicobalt edetate, with a view to providing information that may be of use in cases of poisoning with hydrocyanic acid or cyanides in industry, which now uses these substances in very large quantities.…”

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confidence: 99%

Cobalt Compounds as Antidotes for Hydrocyanic Acid

Evans

1964

British Journal of Pharmacology and Chemotherapy

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The antidotal potency of a cobalt salt (acetate), of dicobalt edetate, of hydroxocobalamin and of cobinamide against hydrocyanic acid was examined mainly on mice and rabbits. All the compounds were active antidotes for up to twice the LD50; under some conditions for larger doses. The most successful was cobalt acetate for rabbits (5 x LD50), which was effective at a molar cyanide/cobalt (CN/Co) ratio of 5, but had as a side-effect intense purgation. Hydroxocobalamin was irregular in action, but on the whole was most effective for mice (4.5 X LDS0 at a molar ratio of 1), and had no apparent side effects. Dicobalt edetate, at molar ratios of up to 2, was more effective for rabbits (3 x LD50) than for mice (2 x LD50), but had fewer side effects than cobalt acetate. The effect of thiosulphate was to augment the efficacy of dicobalt edetate and, in mice, that of hydroxocobalamin; but, apparently, in rabbits, to reduce that of hydroxocobalamin. Cobinamide, at a molar ratio of 1, was slightly more effective than hydroxocobalamin on rabbits and also less irregular in its action. Cobalt acetate by mouth was effective against orally administered hydrocyanic acid. The oxygen uptake of the body, reduced by cyanide, is rapidly reinstated when one of the cobalt antidotes has been successfully administered.Hydrocyanic acid acts as a poison because it combines with, and immobilizes the function of, the iron atom in cytochrome oxidase (derived from cytochrome a3) (Keilin & Hartree, 1939), so blocking the electron transfer through the cytochrome system, and checking the final oxidations involving oxygen uptake of the tricarboxylic acid cycle. It also inhibits many other enzymes, for example, decarboxylases (Blaschko, 1942); these last effects have no recognizable relation to the toxic action.Attempts to find an antidote for cyanide have usually been in the direction of breaking down the cyanide-cytochrome a3 complex, and have looked for substances with a stronger affinity for cyanide ions than has the oxidase. One such method is to convert some of the blood haemoglobin into methaemoglobin, for example, by injection of a nitrite (Paulet, 1959); the methaemoglobin combines with the cyanide ion to form the very stable cyanmethaemoglobin. This has the drawback that it involves the loss of oxygen-carrying power of the blood, so that, for example, to antidote twice the LD50 of cyanide would be equivalent to the loss of about 10% (or in an adult man 450 ml.) of the blood.Since cobalt salts form stable complexes with cyanide, the cobaltocyanides, M4Co(CN)6, and the cobalticyanides, M3Co(CN)6, they have been shown long ago

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Valeur et Mécanisme D'action de L'oxygénothérapie Dans le Traitement de L'intoxication Cyanhydrique

Cited by 12 publications

References 9 publications

Long-Term Neuropsychiatric Sequelae in a Survivor of Cyanide Toxicity Patient With Arterialization

Long-Term Neuropsychiatric Sequelae in a Survivor of Cyanide Toxicity Patient With Arterialization

Clinical pharmacology of systemic antidotes

Cobalt Compounds as Antidotes for Hydrocyanic Acid

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