Neuromuscular Functions on Experimental Acute Methanol Intoxication


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MORAL A. R. , ÇANKAYALI İ. , SERGİN D. , BOYACILAR O.

TURKISH JOURNAL OF ANAESTHESIOLOGY AND REANIMATION, cilt.43, ss.337-343, 2015 (ESCI İndekslerine Giren Dergi) identifier identifier identifier

  • Cilt numarası: 43 Konu: 5
  • Basım Tarihi: 2015
  • Doi Numarası: 10.5152/tjar.2015.13471
  • Dergi Adı: TURKISH JOURNAL OF ANAESTHESIOLOGY AND REANIMATION
  • Sayfa Sayıları: ss.337-343

Özet

Objective: The incidence of accidental or suicidal ingestion of methyl alcohol is high and methyl alcohol intoxication has high mortality. Methyl alcohol intoxication causes severe neurological sequelae and appears to be a significant problem. Methyl alcohol causes acute metabolic acidosis, optic neuropathy leading to permanent blindness, respiratory failure, circulatory failure and death. It is metabolised in the liver, and its metabolite formic acid has direct toxic effects, causing oxidative stress, mitochondrial damage and increased lipid peroxidation associated with the mechanism of neurotoxicity. Methanol is known to cause acute toxicity of the central nervous system; however, the effects on peripheral neuromuscular transmission are unknown. In our study, we aimed to investigate the electrophysiological effects of experimentally induced acute methanol intoxication on neuromuscular transmission in the early period (first 24 h).