疼痛源镇痛的研究和应用

Research and application of attacking pain at its source

目的:阿片治疗严重疼痛因其容易出现中枢性副作用而受限。最近提出作用于疼痛源的镇痛新方法,探讨近年来疼痛源镇痛研究和应用进展。资料来源:应用计算机检索Medline1991-01/2005-12相关疼痛治疗和神经系统的文献,检索词“Pain,therapy,nervesystem”,并限定文献语言种类为English。资料选择:对资料进行初审,选取包括疼痛、治疗和神经系统的文献,开始查找全文。纳入标准:①疼痛与治疗。②疼痛和神经系统。排除标准:①作用于中枢神经系统镇痛。②综述文献、重复研究、Meta分析类文章。资料提炼:共收集到98篇关于疼痛治疗和神经系统的文献,纳入27篇符合标准的文献,3篇文献对疼痛治疗和神经系统进行评价。资料综合:疼痛源镇痛方法包括作用于中枢神经系统以外的受体相关镇痛、以外周受损组织中携带阿片肽的免疫细胞为靶点镇痛和在外周损伤部位基因转染增加阿片肽产生的基因镇痛。急性伤害性、炎症性和神经病理性疼痛在一定程度上有赖于外周初级感觉传入神经元的激活。炎症促进了初级传入神经元中阿片受体的增加,实际上阿片受体正常偶联是发生在轴突还是仅仅发生在神经末梢还不清楚,最后,炎性组织中内源性阿片配体的分泌可能在外周阿片受体中产生相加和协同作用。通过基因治疗来增加损伤组织中阿片肽的合成和释放,被称为外周转阿片肽基因镇痛。结论:疼痛源镇痛是肯定可行的,但其方法有待进一步研究。

OBJECTIVE： The treatment of severe pain with opioid has thus far been limited by their unwanted central side effects, and new method of relieving pain has been put forward recently, The article is aimed at probing into the advances in analgesia attacking pain at its source in recent years. DATA SOURCES： The English literatures on pain relieving and nervous system from January 1991 to December 2005 were searched in Medline by using the key words of ＂pain, therapy, nerve system＂. STUDY SELECTION： Data were checked in the first trial. Literatures related to pain, therapy and nervous system were selected, and the rests were looked for the full text Inclusive criteria： ①pain and therapy.②Pain and nervous system. Exclusive criteria： ①analgesia on central nervous system,②Reviews, repeated studies and Meta analytical papers. DATA EXTRACTION： A total of 98 articles related to pain relieving and nervous system were collected, and 27 enrolled papers were in accordance with the inclusive criteria,, and 3 papers evaluated the pain therapy and nervous system. DATA SYNTHESIS： The methods of analgesia attacking pain at its source included receptor related analgesia acting outside the central nervous system, analgesia aiming at the immune cells of opioid peptide in the peripheral damaged tissues, and gene analgesia produced by opioid owing to the gene-transfection at sites of injury. Pain of acute damage, inflammation and neuropathology were to some extend dependent on the activation of primary-sensory afferent neuron in periphery. The inflammation promoted the increasing of opioid receptor of primary afferent neuron, in fact, whether the normal couple of opioid receptor occurred in axis cylinder or only in the nerve ending was not clear. At last, the secretion of endogenous opioid receptor in inflammations might produce addition and synergistic effects. To increase the synthesis and release of opioid peptide in injured tissue through gene therapy was called periphery transferred opioid peptide gene analgesia. CONCLUSION： It is feasible to conduct analgesics attacking pain at its source. However, more work should be done on the methods.