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Evaluating the effects of rifampin in the prevention of neurogenic symptoms and cardiac arrhythmias caused by the systemic toxicity of lidocaine in rats

Lidocaine toxicity is caused by unintended intravascular injection or overdose. Lidocaine is metabolized in the liver by the CYP3A4 isoenzyme. The objective was to investigate if the administration of rifampin could accelerate animal recovery and reduce the symptoms of lidocaine toxicity by inductio...

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Autores principales: Kazemi-Darabadi, Siamak, Tavakoli, Soodeh, Panahi, Yousef, Akbari, Hamid
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Urmia University Press 2023
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10612392/
https://www.ncbi.nlm.nih.gov/pubmed/37901354
http://dx.doi.org/10.30466/vrf.2022.1985909.3724
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author Kazemi-Darabadi, Siamak
Tavakoli, Soodeh
Panahi, Yousef
Akbari, Hamid
author_facet Kazemi-Darabadi, Siamak
Tavakoli, Soodeh
Panahi, Yousef
Akbari, Hamid
author_sort Kazemi-Darabadi, Siamak
collection PubMed
description Lidocaine toxicity is caused by unintended intravascular injection or overdose. Lidocaine is metabolized in the liver by the CYP3A4 isoenzyme. The objective was to investigate if the administration of rifampin could accelerate animal recovery and reduce the symptoms of lidocaine toxicity by induction of the CYP3A4. Thirty-six male rats were divided into control and treatment groups, each containing three subgroups. The treatment group received oral rifampin suspension daily for 1 week. In all rats, 2.00% lidocaine was injected intravenously. The first subgroup was monitored for neurological symptoms. In the second subgroup, data were recorded after the electrode was placed in the right hippocampus. Electrocardiograms were taken from the third subgroup. CYP3A4 was measured using an ELISA kit. Neurological recovery was seen after 22 and 15 min in the control and treatment groups, respectively. Rifampin also caused a significant reduction in amplitude and number of field action potentials compared to the control group. Numerous cardiac arrhythmias were observed in the control group. The mean level of CYP3A4 in the treatment group was significantly higher than in the control group. In conclusion, oral rifampin could increase the synthesis of CYP3A4, therefore, the animal recovery from lidocaine toxicity was accelerated.
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spelling pubmed-106123922023-10-29 Evaluating the effects of rifampin in the prevention of neurogenic symptoms and cardiac arrhythmias caused by the systemic toxicity of lidocaine in rats Kazemi-Darabadi, Siamak Tavakoli, Soodeh Panahi, Yousef Akbari, Hamid Vet Res Forum Original Article Lidocaine toxicity is caused by unintended intravascular injection or overdose. Lidocaine is metabolized in the liver by the CYP3A4 isoenzyme. The objective was to investigate if the administration of rifampin could accelerate animal recovery and reduce the symptoms of lidocaine toxicity by induction of the CYP3A4. Thirty-six male rats were divided into control and treatment groups, each containing three subgroups. The treatment group received oral rifampin suspension daily for 1 week. In all rats, 2.00% lidocaine was injected intravenously. The first subgroup was monitored for neurological symptoms. In the second subgroup, data were recorded after the electrode was placed in the right hippocampus. Electrocardiograms were taken from the third subgroup. CYP3A4 was measured using an ELISA kit. Neurological recovery was seen after 22 and 15 min in the control and treatment groups, respectively. Rifampin also caused a significant reduction in amplitude and number of field action potentials compared to the control group. Numerous cardiac arrhythmias were observed in the control group. The mean level of CYP3A4 in the treatment group was significantly higher than in the control group. In conclusion, oral rifampin could increase the synthesis of CYP3A4, therefore, the animal recovery from lidocaine toxicity was accelerated. Urmia University Press 2023 2023-10-15 /pmc/articles/PMC10612392/ /pubmed/37901354 http://dx.doi.org/10.30466/vrf.2022.1985909.3724 Text en © 2023 Urmia University. All rights reserved https://creativecommons.org/licenses/by-nc-sa/4.0/This work is licensed under a Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) (https://creativecommons.org/licenses/by-nc-sa/4.0 (https://creativecommons.org/licenses/by-nc-sa/4.0/) )which allows users to read, copy, distribute and make derivative works for non-commercial purposes from the material, as long as the author of the original work is cited properly.
spellingShingle Original Article
Kazemi-Darabadi, Siamak
Tavakoli, Soodeh
Panahi, Yousef
Akbari, Hamid
Evaluating the effects of rifampin in the prevention of neurogenic symptoms and cardiac arrhythmias caused by the systemic toxicity of lidocaine in rats
title Evaluating the effects of rifampin in the prevention of neurogenic symptoms and cardiac arrhythmias caused by the systemic toxicity of lidocaine in rats
title_full Evaluating the effects of rifampin in the prevention of neurogenic symptoms and cardiac arrhythmias caused by the systemic toxicity of lidocaine in rats
title_fullStr Evaluating the effects of rifampin in the prevention of neurogenic symptoms and cardiac arrhythmias caused by the systemic toxicity of lidocaine in rats
title_full_unstemmed Evaluating the effects of rifampin in the prevention of neurogenic symptoms and cardiac arrhythmias caused by the systemic toxicity of lidocaine in rats
title_short Evaluating the effects of rifampin in the prevention of neurogenic symptoms and cardiac arrhythmias caused by the systemic toxicity of lidocaine in rats
title_sort evaluating the effects of rifampin in the prevention of neurogenic symptoms and cardiac arrhythmias caused by the systemic toxicity of lidocaine in rats
topic Original Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10612392/
https://www.ncbi.nlm.nih.gov/pubmed/37901354
http://dx.doi.org/10.30466/vrf.2022.1985909.3724
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