Cerebral energy metabolism in cyanide encephalopathy.
This study documents the effects of an intracarotid artery injection of a lethal threshold amount of KCN (2.5 mg.kg-1) on the energy metabolism and histology of the rat brain. This dose of KCN resulted in a rapid abolition of electroencephalographic activity, which remained essentially absent for up to 3 h. Cerebral metabolite measurements 0.25 h after KCN infusion indicated a 52% reduction in cytochrome oxidase activity, a 600% increase in lactate, a 32% reduction in ATP, a 73% increase in ADP, and an 85% decrease in glycogen. Measurements of the above energy metabolites over the ensuing 7 days showed a return to control of all metabolites by 6-24 h. Corresponding to the normalization of energy metabolism was a return of EEG and conscious activity. Histological examination of cyanide-exposed animals revealed a paucity of change with only one animal at 0.5 h showing several dark neurons, two animals at 1 h with minor pallor of corpus callosum and caudate-putamen, and one animal at 48 h with a small hippocampal infarction. It is concluded that it may be impossible to produce a serious enough disruption of cerebral metabolism with KCN injection, to produce neuronal damage by purely "histotoxic" mechanisms.
MacMillan
V H
VH
Department of Medicine, University of Toronto, Ontario, Canada.
D000818:Animals; D001794:Blood Pressure; D001927:Brain Diseases / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D003486:Cyanides / Q000009:adverse effects*; D004569:Electroencephalography; D004734:Energy Metabolism; D008297:Male; D011190:Potassium Cyanide / Q000009:adverse effects*; D051381:Rats; D011919:Rats, Inbred Strains
D003486:Cyanides; D011190:Potassium Cyanide