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地塞米松对电针镇痛及中枢神经系统代谢的影响。

Effects of dexamethasone on electroacupuncture analgesia and central nervous system metabolism.

作者信息

Liu J Z, Huang Y H, Hand P J

机构信息

Department of Animal Biology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia 19104.

出版信息

Acupunct Electrother Res. 1988;13(1):9-23. doi: 10.3727/036012988816358769.

DOI:10.3727/036012988816358769
PMID:2898201
Abstract

Many reports have indicated that electro-acupuncture analgesia (EAA) was mediated by endorphins. Among them is B-endorphin which can be released from the anterior lobe of the pituitary. To examine the role of B-endorphin in EAA and observe CNS metabolic (functional) and behavioral effects of dexamethasone the present study employed the (14C) 2-deoxyglycose (2DG) method. Seventeen adult male Sprague-Dawley rats in five groups received the following different types of somesthetic stimulation to examine the local cerebral glucose utilization (LCGU) and tail-flick response latency: control group (N = 3), pain group (N = 4), EA group (N = 3), pain + EA group (N = 3; from another ongoing study) and dexamethasone group (N = 4). Dexamethasone reduced tail-flick response latency in response to electroacupuncture, and produced metabolic (functional) changes in a number of CNS structures implicated in electroacupuncture produced analgesia effects (some changes were statistically significant, many others were not). Specific brain structures exhibiting statistically significant changes (p less than 0.05) in LCGU when compared to the pain + EA group are: the parafascicular and habennlar nuclei of the thalamus and the posterior cingulate gyrus. In comparison of dexamethasone group with the other four experimental groups of rats, the following trend in LCGU changes was observed: pain + EA group greater than pain group = EA group = dexamethasone group greater than control group. In addition, dexamethasone had a sedative effect. The results suggest that dexamethasone is reducing EAA and having suppressive effects on CNS metabolism and behavior.

摘要

许多报告表明,电针镇痛(EAA)是由内啡肽介导的。其中β-内啡肽可从垂体前叶释放。为了研究β-内啡肽在电针镇痛中的作用,并观察地塞米松对中枢神经系统代谢(功能)和行为的影响,本研究采用了(14C)2-脱氧葡萄糖(2DG)方法。17只成年雄性Sprague-Dawley大鼠分为五组,接受以下不同类型的躯体感觉刺激,以检测局部脑葡萄糖利用率(LCGU)和甩尾反应潜伏期:对照组(N = 3)、疼痛组(N = 4)、电针组(N = 3)、疼痛+电针组(N = 3;来自另一项正在进行的研究)和地塞米松组(N = 4)。地塞米松缩短了电针刺激引起的甩尾反应潜伏期,并在一些与电针镇痛效应相关的中枢神经系统结构中产生了代谢(功能)变化(一些变化具有统计学意义,许多其他变化则没有)。与疼痛+电针组相比,在LCGU方面表现出统计学显著变化(p小于0.05)的特定脑结构有:丘脑的束旁核和缰核以及后扣带回。将地塞米松组与其他四组大鼠实验组进行比较,观察到LCGU变化的以下趋势:疼痛+电针组大于疼痛组=电针组=地塞米松组大于对照组。此外,地塞米松有镇静作用。结果表明,地塞米松正在降低电针镇痛效果,并对中枢神经系统代谢和行为产生抑制作用。

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