Lidocaine injection into sciatic nerve induce abnormal sodium channel expression

碩士 === 高雄醫學大學 === 醫學研究所 === 100 === Background: Peripheral nerve injury may cause by disease, surgery or unintentionally intraneural injections of medicines. Lidocaine, a local anesthetic and an anti-arrhythmic agent, is most commonly administered for neuraxial anesthesia or peripheral nerve block....

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Main Authors: Chao-Wen Chou, 周昭彣
Other Authors: Lin-Li Chang
Format: Others
Language:zh-TW
Published: 2012
Online Access:http://ndltd.ncl.edu.tw/handle/85498273834556564084
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spelling ndltd-TW-100KMC055340172015-10-13T21:55:42Z http://ndltd.ncl.edu.tw/handle/85498273834556564084 Lidocaine injection into sciatic nerve induce abnormal sodium channel expression 注射Lidocaine於坐骨神經會誘發鈉離子通道異常表現 Chao-Wen Chou 周昭彣 碩士 高雄醫學大學 醫學研究所 100 Background: Peripheral nerve injury may cause by disease, surgery or unintentionally intraneural injections of medicines. Lidocaine, a local anesthetic and an anti-arrhythmic agent, is most commonly administered for neuraxial anesthesia or peripheral nerve block. However, it still causes nerve damage following intraneural injection. Aim: In the present study, lidocaine was intraneural administration into sciatic nerve in order to investigate lidocaine lintraneurally induced pains,dys-regulation of f voltage-gated sodium channels (VGSCs) in dorsal root ganglion and microglia activation in spinal dorsal horn. Materials and methods: Sprague-Dawley (SD) rats were randomly divided into two groups: (1) naive group, no surgery or treatment was received; (2) experimental group, 0.1 ml 2% lidocaine left sciatic nerve intraneural injection was given. Neuropathic pain was assessed based on behavioral responses to thermal and mechanical stimuli. Expression of sodium channels (Nav1.3, 1.6, 1.7and Nav1.8) in injured sciatic nerve as well as dorsal root ganglia, and microglial proliferation/activation in the spinal cord were measured following nerve injury of 6, 12, 24, 36, 48 hours and 3, 7, 14 days, respectively. Results: in experimental rats showed of mechanical allodynia rapidly 6 hrs afterintraneural lidocaine injectionand it persisted for 14 days. Activated Microglia increased intensity on day 4, to reach peak on day 7 then returned to normal level on 14 days. Up-regulated expression of VGSCs in injured sciatic nerve segment appeared significantly within 24 hours. After then, up-regulated Nav1.3 and down-regulated Nav1.8 in DRGs at 36 hours was observed. However, only the Nav1.8 lasted its abnormal expression for 14 days. Conclusion: rats with nerve injury caused by intraneural lidocaine injection suffer from mechanical allodyniait is closely associated with down-regulated expression of Nav1.8 in injured DRGs and increased intensity of activated microglia shown on spinal dorsal horn. Lin-Li Chang 張玲麗 2012 學位論文 ; thesis 55 zh-TW
collection NDLTD
language zh-TW
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description 碩士 === 高雄醫學大學 === 醫學研究所 === 100 === Background: Peripheral nerve injury may cause by disease, surgery or unintentionally intraneural injections of medicines. Lidocaine, a local anesthetic and an anti-arrhythmic agent, is most commonly administered for neuraxial anesthesia or peripheral nerve block. However, it still causes nerve damage following intraneural injection. Aim: In the present study, lidocaine was intraneural administration into sciatic nerve in order to investigate lidocaine lintraneurally induced pains,dys-regulation of f voltage-gated sodium channels (VGSCs) in dorsal root ganglion and microglia activation in spinal dorsal horn. Materials and methods: Sprague-Dawley (SD) rats were randomly divided into two groups: (1) naive group, no surgery or treatment was received; (2) experimental group, 0.1 ml 2% lidocaine left sciatic nerve intraneural injection was given. Neuropathic pain was assessed based on behavioral responses to thermal and mechanical stimuli. Expression of sodium channels (Nav1.3, 1.6, 1.7and Nav1.8) in injured sciatic nerve as well as dorsal root ganglia, and microglial proliferation/activation in the spinal cord were measured following nerve injury of 6, 12, 24, 36, 48 hours and 3, 7, 14 days, respectively. Results: in experimental rats showed of mechanical allodynia rapidly 6 hrs afterintraneural lidocaine injectionand it persisted for 14 days. Activated Microglia increased intensity on day 4, to reach peak on day 7 then returned to normal level on 14 days. Up-regulated expression of VGSCs in injured sciatic nerve segment appeared significantly within 24 hours. After then, up-regulated Nav1.3 and down-regulated Nav1.8 in DRGs at 36 hours was observed. However, only the Nav1.8 lasted its abnormal expression for 14 days. Conclusion: rats with nerve injury caused by intraneural lidocaine injection suffer from mechanical allodyniait is closely associated with down-regulated expression of Nav1.8 in injured DRGs and increased intensity of activated microglia shown on spinal dorsal horn.
author2 Lin-Li Chang
author_facet Lin-Li Chang
Chao-Wen Chou
周昭彣
author Chao-Wen Chou
周昭彣
spellingShingle Chao-Wen Chou
周昭彣
Lidocaine injection into sciatic nerve induce abnormal sodium channel expression
author_sort Chao-Wen Chou
title Lidocaine injection into sciatic nerve induce abnormal sodium channel expression
title_short Lidocaine injection into sciatic nerve induce abnormal sodium channel expression
title_full Lidocaine injection into sciatic nerve induce abnormal sodium channel expression
title_fullStr Lidocaine injection into sciatic nerve induce abnormal sodium channel expression
title_full_unstemmed Lidocaine injection into sciatic nerve induce abnormal sodium channel expression
title_sort lidocaine injection into sciatic nerve induce abnormal sodium channel expression
publishDate 2012
url http://ndltd.ncl.edu.tw/handle/85498273834556564084
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AT chaowenchou zhùshèlidocaineyúzuògǔshénjīnghuìyòufānàlízitōngdàoyìchángbiǎoxiàn
AT zhōuzhāowén zhùshèlidocaineyúzuògǔshénjīnghuìyòufānàlízitōngdàoyìchángbiǎoxiàn
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