Neuromuscular functions on experimental acute methanol intoxication

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dc.contributor.authorMoral A.R.
dc.contributor.authorÇankayalı İ.
dc.contributor.authorSergin D.
dc.contributor.authorBoyacılar Ö.
dc.date.accessioned2019-10-26T21:21:39Z
dc.date.available2019-10-26T21:21:39Z
dc.date.issued2015
dc.departmentEge Üniversitesien_US
dc.description.abstractObjective: 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). Methods: After approval by the Animal Experiment Ethics Committee of Ege University, the study was carried out on 10 Wistar rats, each weighing about 200 g. During electrophysiological recordings and orogastric tube insertion, the rats were anaesthetised using intra-peritoneal (IP) injection of ketamine 100 mg kg-1 and IP injection of xylazine 10 mg kg-1. The rats were given 3 g kg-1 methyl alcohol by the orogastric tube. Electrophysiological measurements from the gastrocnemius muscle were compared with baseline. Results: Latency measurements before and 24 h after methanol injection were 0.81±0.11 ms and 0.76±0.12 ms, respectively. CMAP amplitude measurements before and 24 h after methanol injection were 9.85±0.98 mV and 9.99±0.40 mV, respectively. CMAP duration measurements before and 24 h after methanol injection were 9.86±0.03 ms and 9.86±0.045 ms, respectively. Conclusion: It was concluded that experimental methanol intoxication in the acute phase (first 24 h) did not affect neuromuscular function. © 2015 by Turkish Anaesthesiology and Intensive Care Society.en_US
dc.identifier.doi10.5152/TJAR.2015.13471
dc.identifier.endpage343en_US
dc.identifier.issn1304-0871
dc.identifier.issn1304-0871en_US
dc.identifier.issue5en_US
dc.identifier.scopusqualityN/Aen_US
dc.identifier.startpage337en_US
dc.identifier.urihttps://doi.org/10.5152/TJAR.2015.13471
dc.identifier.urihttps://hdl.handle.net/11454/16894
dc.identifier.volume43en_US
dc.indekslendigikaynakScopusen_US
dc.language.isoenen_US
dc.publisherAVES İbrahim KARAen_US
dc.relation.ispartofTurk Anesteziyoloji ve Reanimasyon Dernegi Dergisien_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US
dc.rightsinfo:eu-repo/semantics/openAccessen_US
dc.subjectIntoxicationen_US
dc.subjectMethanolen_US
dc.subjectNeuromuscular transmissionen_US
dc.subjectPolyneuropathyen_US
dc.titleNeuromuscular functions on experimental acute methanol intoxicationen_US
dc.typeArticleen_US

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