The role of hypothermia 35 °c in lidocaine-induced neurotoxicity

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Background: Lidocaine in spinal anesthesia may cause nerve injury and has been related to increase incidence of cauda equina syndrome and persistent lumbosacral neuropathy after spinal anesthesia. Lidocaine neurotoxicity involves necrosis process and mitochondrial dysfunction followed by activation of intrinsic apoptotic pathways. Therapeutic mild hypothermia is a new treatment, which increases survival chances and quality of life in ischemic nerve injury patients. The aim of this study is to obtain information about the role of mild hypothermia (35 °C) in lidocaine induced neurotoxicity. Methods: In human neuroblastoma SH-SY5Y cells, viability of cells after various concentrations of lidocaine exposure in 37 °C and 35 °C was quantitatively determined by MTT colorimetric assay. Image based cytometer was also used to determine quantitatively percentage of necrotic, apoptotic and viable cells. In addition, an antiapoptotic factor, Bcl-2 was assessed by measuring its concentration using solid phase ELISA assay. Results: Lidocaine-induced cell death occurred in dose dependent manner. More than 50% cell death was caused by necrosis process. There is no significant increase of IC50 value of lidocaine, Bcl-2 concentration and cell viability after exposure to hypothermia 35 °C compared with 37 °C. Conclusion: Hypothermia 35 °C did not improve neuroblastoma cells viability treated with lidocaine.

Original languageEnglish
Pages (from-to)6811-6816
Number of pages6
JournalAdvanced Science Letters
Issue number7
Publication statusPublished - Jul 2017


  • Apoptosis
  • Lidocaine exposure
  • Lidocaine neurotoxicity
  • Mild hypothermia
  • Necrosis


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