阿米替林对脊髓电刺激治疗幻肢痛疗效的影响

目的:本研究旨在探讨阿米替林干预对脊髓电刺激(SCS)治疗幻肢痛疗效的影响。方法:研究对象为2007年1月至2009年6月在我科行SCS置入术且符合入组标准并自愿参加研究的幻肢痛患者,共获7例。术后SCS均开启,阿米替林治疗在术后1个月时开始。疼痛、情绪、生活质量评估采用视觉模拟评分法(visualanaloguescales,VAS法),现时疼痛强度评分法(presentpainin-tensity,PPI),综合性医院焦虑抑郁量表(The Hospital Anxiety and Depression Scale,HAD),疼痛失能指数(Pain disability index,PDI)。结果:(1)开启SCS后患者的疼痛、抑郁焦虑情绪及生活质量均得到显著改善。(2)所有患者在使用阿米替林治疗以后疼痛、情绪及生活质量也显著改善。结论:阿米替林能显著提高SCS对幻肢痛的疗效。     

阿米替林对脊髓电刺激治疗幻肢痛疗效的影响

目的：本研究旨在探讨阿米替林干预对脊髓电刺激（SCS）治疗幻肢痛疗效的影响。方法：研究对象为2007年1月至2009年6月在我科行SCS置入术且符合入组标准并自愿参加研究的幻肢痛患者,共获7例。术后SCS均开启,阿米替林治疗在术后1个月时开始。疼痛、情绪、生活质量评估采用视觉模拟评分法（visual analogue scales,VAS法）,现时疼痛强度评分法（presentpain intensity。PPI）,综合性医院焦虑抑郁量表（The Hospital Anxiety and Depression Scale,HAD）,疼痛失能指数（Pain disability index,PDI）。结果：（1）开启SCS后患者的疼痛、抑郁焦虑情绪及生活质量均得到显著改善。（2）所有患者在使用阿米替林治疗以后疼痛、情绪及生活质量也显著改善。结论：阿米替林能显著提高SCS对幻肢痛的疗效。     

T型钙通道在神经病理性痛模型中介导疼痛的研究进展

神经病理痛是临床上常见病症,其发病机制尚不清楚,目前尚无有效的治疗手段,其慢性神经病理痛持续时间长,故其研究成为疼痛领域的热点和重点。近年来发现T型钙通道在神经病理性疼痛中起到了关键性的作用。本文将近年T型钙通道在神经病理性痛模型中介导疼痛的机制研究进展加以综述。     

P2X受体在CCI模型中介导疼痛的研究进展

神经病理痛是临床上常见病症,对人身心健康危害较大,其发病机制尚不清楚,目前无有效的治疗手段,加之慢性神经病理痛持续时间长,其研究成为疼痛领域的热点和重点.本文将围绕着P2X受体在CCI模型中介导疼痛方面的研究加以归纳和总结.     

下行易化系统及其参与神经病理痛的机制

神经病理痛是指由中枢或外周神经系统损伤或疾病引起的疼痛综合征.神经病理痛是临床上常见的一种疾病,但是其发病机制不甚清楚,临床上也缺乏有效的治疗手段.近年来的研究除了集中于痛觉的上行传导及中枢机制,以及痛觉的下行抑制之外,也证明下行易化系统激活参与神经病理痛的发病机制.本文拟对此进行综述,希望为治疗神经病理痛提供新思路.     

神经病理性疼痛研究进展

神经病理胜疼痛是指神经系统的损伤或功能障碍引起的疼痛,占到了各类慢性疼痛的30%以上。第四军医大学完成的—项研究成果成功揭示了神经病理性痛的发生机制,创建两种能够分别模拟神经病理性痛不同临床表现的动物模型为研究神经病理性痛和制定治疗策略奠定了基础。     

肾上腺髓质素在炎性疼痛和吗啡耐受中的作用

背根神经节(dorsal root ganglia,DRG)和脊髓背角中痛介质(pronociceptive mediator)的增加是炎性疼痛与阿片耐受发生的重要病理机制。肾上腺髓质素(adrenomedullin,AM)属于降钙素基因相关肽(calcitonin gene-related peptide,CGRP)家族,是新近证实的痛介质。研究表明,炎症和重复应用吗啡时,DRG和脊髓背角中AM含量和释放都增加。鞘内给予AM受体阻断剂AM22-52能抑制炎性疼痛与吗啡耐受,表明DRG和脊髓背角中AM受体活动的增加参与炎性疼痛和吗啡耐受发生的病理过程。本文综述了最近有关研究进展,讨论了AM参与这两类疾患发生的神经学机制。     

痛觉相关钠离子通道研究进展

疼痛是一种与组织损伤或潜在的损伤相关的不愉快的主观感觉和情感体验,是机体受到伤害性刺激后产生的一种防御反应。伤害性感觉神经元细胞膜上的电压门控钠离子通道是细胞表面一类跨膜糖蛋白,负责可兴奋细胞动作电位的产生和传导,并且在炎性痛、神经病理性疼痛和功能性痛的产生、传导以及维持上起到了重要的作用,成为近年来疼痛病理生理机制研究和疼痛治疗的分子靶标。本文将就痛觉相关钠离子通道的类型,结构,及其表达和功能的改变与疼痛的关系进行综述。     

钙调蛋白激酶Ⅱ在神经病理痛中的作用及其痛觉调控通路概况

钙调蛋白激酶Ⅱ(Ca^2+/calmodulin-dependent protein kinase,CaMKⅡ)是一种多功能的丝氨酸/苏氨酸蛋白激酶,在神经元中大量存在,广泛参与疼痛调制。神经病理痛是一种由疾病或躯体感觉系统的损伤引起的慢性难治性疼痛。钙调蛋白激酶Ⅱ在中枢、外周神经病理痛、代谢型神经病理痛和药物引起神经病理痛等各种类型的神经病理痛的发生发展中发挥着重要的作用。本文拟将从钙调激酶Ⅱ介导的各型神经病理痛及其上下游的调控两个方面进行综述,以期为今后钙调蛋白激酶Ⅱ在神经病理痛领域的研究提供一定参考。     

癌痛的分子机理研究进展

疼痛是肿瘤患者的常见并发症。癌痛的产生不同于炎性痛和神经病理性疼痛。动物模型的构建能帮助我们更好地了解癌痛的分子调控机制。随着对癌痛机制的进一步研究,未来针对性的靶点镇痛治疗指日可待。本文就研究癌痛的动物模型及癌痛产生的相关分子机制等方面的进展进行综述。     

Investigation of the mechanism of temperature sensitivity of the electroreceptors of ampullae of lorenzini

In experiments on Black Sea skates (Raja clavata), the potential of the receptor epithelium of the ampullae of Lorenzini and spike activity of single nerve fibers connected to them were investigated during electrical and temperature stimulation. Usually the potential within the canal was between 0 and –2 mV, and the input resistance of the ampulla 250–400 k. Heating of the region of the receptor epithelium was accompanied by a negative wave of potential, an increase in input resistance, and inhibition of spike activity. With worsening of the animal's condition the transepithelial potential became positive (up to +10 mV) but the input resistance of the ampulla during stimulation with a positive current was nonlinear in some cases: a regenerative spike of positive polarity appeared in the channel. During heating, the spike response was sometimes reversed in sign. It is suggested that fluctuations of the transepithelial potential and spike responses to temperature stimulation reflect changes in the potential difference on the basal membrane of the receptor cells, which is described by a relationship of the Nernst's or Goldman's equation type.I. P. Pavlov Institute of Physiology, Academy of Sciences of the USSR, Leningrad. I. M. Sechenov, Institute of Evolutionary Physiology and Biochemistry, Academy of Sciences of the USSR, Leningrad. Pacific Institute of Oceanology, Far Eastern Scientific Center, Academy of Sciences of the USSR, Vladivostok. Translated from Neirofiziologiya, Vol. 12, No. 1, pp. 67–74, January–February, 1980.     

Principles of organization and evolution of systems of regulation of functions

Evolution of living organisms is closely connected with evolution of structure of the system of regulations and its mechanisms. The functional ground of regulations is chemical signalization. As early as in unicellular organisms there is a set of signal mechanisms providing their life activity and orientation in space and time. Subsequent evolution of ways of chemical signalization followed the way of development of delivery pathways of chemical signal and development of mechanisms of its regulation. The mechanism of chemical regulation of the signal interaction is discussed by the example of the specialized system of transduction of signal from neuron to neuron, of effect of hormone on the epithelial cell and modulation of this effect. These mechanisms are considered as the most important ways of the fine and precise adaptation of chemical signalization underlying functioning of physiological systems and organs of the living organism