致命氰化物中毒的代谢效应。
The metabolic effects of fatal cyanide poisoning.
作者信息
Singh B M, Coles N, Lewis P, Braithwaite R A, Nattrass M, FitzGerald M G
机构信息
General Hospital, Birmingham, UK.
出版信息
Postgrad Med J. 1989 Dec;65(770):923-5. doi: 10.1136/pgmj.65.770.923.
Metabolic and toxicological data were obtained during the first 24 hours following severe and eventually fatal cyanide poisoning. Initial blood cyanide concentrations were 804 mumol/l but fell rapidly over 24 hours following cobalt edetate therapy to 15 mumol/l. However, plasma thiocyanate concentrations rose over 24 hours (147-267 mumol/l) suggesting continued tissue detoxification. The major metabolic abnormality was lactic acidosis (initial pH 7.21, blood lactate 17.5 mmol/l) which corrected over 12 hours. Despite high circulating insulin concentrations the responses of blood glucose, plasma non-esterified fatty acid, blood glycerol and 3-hydroxybutyrate suggested marked insulin resistance.
在严重且最终致命的氰化物中毒后的最初24小时内获取了代谢和毒理学数据。初始血氰浓度为804μmol/L，但在依地酸钴治疗后的24小时内迅速降至15μmol/L。然而，血浆硫氰酸盐浓度在24小时内升高（147 - 267μmol/L），提示组织持续进行解毒。主要的代谢异常是乳酸酸中毒（初始pH 7.21，血乳酸17.5mmol/L），其在12小时内得到纠正。尽管循环胰岛素浓度很高，但血糖、血浆非酯化脂肪酸、血甘油和3 - 羟基丁酸的反应提示存在明显的胰岛素抵抗。
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