Suppr超能文献

早期和晚期糖尿病神经病变对 Zucker 糖尿病肥胖大鼠坐骨神经阻滞持续时间和神经毒性的影响。

Effects of early and late diabetic neuropathy on sciatic nerve block duration and neurotoxicity in Zucker diabetic fatty rats.

机构信息

Department of Anaesthesiology and Laboratory of Experimental Anaesthesiology and Intensive Care (LEICA), University of Amsterdam, Amsterdam, The Netherlands.

Department of Neurology, Academic Medical Center, University of Amsterdam, Amsterdam, The Netherlands.

出版信息

Br J Anaesth. 2015 Feb;114(2):319-26. doi: 10.1093/bja/aeu270. Epub 2014 Aug 21.

Abstract

BACKGROUND

The neuropathy of type II diabetes mellitus (DM) is increasing in prevalence worldwide. We aimed to test the hypothesis that in a rodent model of type II DM, neuropathy would lead to increased neurotoxicity and block duration after lidocaine-induced sciatic nerve block when compared with control animals.

METHODS

Experiments were carried out in Zucker diabetic fatty rats aged 10 weeks (early diabetic) or 18 weeks (late diabetic, with or without insulin 3 units per day), and age-matched healthy controls. Left sciatic nerve block was performed using 0.2 ml lidocaine 2%. Nerve conduction velocity (NCV) and F-wave latency were used to quantify nerve function before, and 1 week after nerve block, after which sciatic nerves were used for neurohistopathology.

RESULTS

Early diabetic animals did not show increased signs of nerve dysfunction after nerve block. In late diabetic animals without insulin vs control animals, NCV was 34.8 (5.0) vs 41.1 (4.1) ms s(-1) (P<0.01), and F-wave latency was 7.7 (0.5) vs 7.0 (0.2) ms (P<0.01), respectively. Motor nerve block duration was prolonged in late diabetic animals, but neurotoxicity was not. Late diabetic animals receiving insulin showed intermediate results.

CONCLUSIONS

In a rodent type II DM model, nerves have increased sensitivity for short-acting local anaesthetics without adjuvants in vivo, as evidenced by prolonged block duration. This sensitivity appears to increase with the progression of neuropathy. Our results do not support the hypothesis that neuropathy due to type II DM increases the risk of nerve injury after nerve block.

摘要

背景

全球范围内,2 型糖尿病(DM)相关神经病变的发病率呈上升趋势。我们旨在验证以下假说,即在 2 型 DM 啮齿动物模型中,与对照动物相比,神经病变会导致利多卡因坐骨神经阻滞后神经毒性和阻滞时间延长。

方法

在 10 周龄(早期糖尿病)或 18 周龄(晚期糖尿病,每日给予或不给予 3 单位胰岛素)的 Zucker 糖尿病肥胖大鼠及年龄匹配的健康对照中进行实验。采用 0.2 ml 2%利多卡因行左侧坐骨神经阻滞。神经传导速度(NCV)和 F 波潜伏期用于在神经阻滞前和 1 周后(神经阻滞后)定量神经功能,之后用于神经组织病理学检查。

结果

早期糖尿病动物神经阻滞后未出现神经功能障碍加重的迹象。晚期糖尿病未接受胰岛素治疗的动物与对照组相比,NCV 分别为 34.8(5.0)ms s(-1)和 41.1(4.1)ms s(-1)(P<0.01),F 波潜伏期分别为 7.7(0.5)ms 和 7.0(0.2)ms(P<0.01)。晚期糖尿病动物的运动神经阻滞时间延长,但无神经毒性。接受胰岛素治疗的晚期糖尿病动物表现出中间结果。

结论

在 2 型 DM 啮齿动物模型中,体内无佐剂的短时效局麻药使神经敏感性增加,表现为阻滞时间延长。这种敏感性似乎随着神经病变的进展而增加。我们的结果不支持 2 型 DM 引起的神经病变会增加神经阻滞后神经损伤风险的假说。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验