PMID: 7337499Dec 1, 1981Paper

Behavioural, electroencephalographic and histological study of the protective effect of etomidate against histotoxic dysoxia produced by cyanide

Archives Internationales De Pharmacodynamie Et De Thérapie
D AshtonA Wauquier

Abstract

The acute toxicity of cyanide is largely due to the inhibition of cytochrome oxidase, and the subsequent breakdown of cellular metabolism. Breakdown in cellular metabolism, leading to a disruption of cellular integrity lies at the heart of the permanent neurological damage resulting from ischemic/hypoxic brain insult. In 200 g male Wistar rats treated with 5 mg/kg KCN i.v. and ventilated until spontaneous breathing restarted, the cornea reflex, tail-pinch reaction and righting reflex disappeared for about 20 min. In curarized and artificially ventilated rats the EEG remained flat for a similar period before slowly returning. Saline treated animals which survive the KCN injection die significantly earlier than non-KCN treated animals when injected with 120 mg/kg metrazol s.c. one week later. Histological examination of KCN treated animals revealed swollen mitochondria at 20 min, and microvacuolization and ischemic cell changes at 1 week. In rats pretreated with etomidate 10 mg/kg s.c. 30 min before cyanide the cornea, tail-pinch and righting reflex were absent for the same time as in controls. The EEG was similar to that seen in saline/KCN animals, however, the time to EEG was similar to that seen in saline/KCN animals, however,...Continue Reading

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