本文選題：病理性痛　切入點(diǎn)：蛇毒　出處：《第四軍醫(yī)大學(xué)》2006年博士論文　論文類型：學(xué)位論文

【摘要】：疼痛是一種復(fù)雜的生理心理活動(dòng)，是臨床上最常見的癥狀之一。它包括傷害性刺激作用于機(jī)體所引起的痛感覺，以及機(jī)體對(duì)傷害性刺激的痛反應(yīng)。臨床病理性痛可表現(xiàn)為持續(xù)性的自發(fā)痛及伴有長(zhǎng)時(shí)程持續(xù)性痛敏和觸誘發(fā)痛現(xiàn)象。闡明病理性痛的發(fā)生和慢性化機(jī)制在很大程度上依賴于能夠模擬臨床病理性痛特征的動(dòng)物模型的深入研究。目前常用的病理性痛機(jī)制研究的模型有福爾馬林試驗(yàn)?zāi)Ｐ�、完全弗氏佐劑模型、坐骨神�?jīng)部分結(jié)扎模型和坐骨神經(jīng)慢性壓迫模型等。至今，，新的病理性痛的模型還在不斷的開發(fā)和探索中，原因即在于上述動(dòng)物疼痛模型雖然各有特點(diǎn)，但亦有其局限性，不能完全模擬病理痛的特征。 近些年來，利用動(dòng)物毒素致痛模擬病理性痛癥狀來探索痛信息傳遞與調(diào)控的機(jī)制的研究逐漸增多。本研究中利用外周給與動(dòng)物毒素致痛的模型來探討動(dòng)物毒素誘致痛敏發(fā)生的神經(jīng)機(jī)制。本研究包含以下兩部分內(nèi)容： 1、本課題聯(lián)合應(yīng)用形態(tài)學(xué)和行為藥理學(xué)方法觀察了坐骨神經(jīng)內(nèi)注射蛇毒(SV)誘致痛敏的神經(jīng)機(jī)制。結(jié)果如下： ①坐骨神經(jīng)內(nèi)注射SV導(dǎo)致坐骨神經(jīng)發(fā)生脫髓鞘(demyelination)現(xiàn)象。注射后2周坐骨神經(jīng)髓鞘的改變最為明顯，接受NS注射的對(duì)照組坐骨神經(jīng)未見明顯改變。 ②坐骨神經(jīng)部分結(jié)扎組手術(shù)側(cè)脊髓內(nèi)P物質(zhì)(SP)、降鈣素基因相關(guān)肽(CGRP)、甘丙肽(GAL)和Ⅰ型囊泡膜谷氨酸轉(zhuǎn)運(yùn)體(VGluT1)的表達(dá)均明顯低于對(duì)照側(cè)。SV致痛后注射側(cè)脊髓內(nèi)SP、CGRP、GAL和無髓纖維
[Abstract]:Pain is a complex physiological and psychological activity that is one of the most common clinical symptoms. It includes painful feelings caused by noxious stimuli acting on the body. The clinical pathological pain can be manifested as persistent spontaneous pain, persistent pain with long-term pain and touch-induced pain. The occurrence and chronic mechanism of pathological pain are explained in this paper. The degree depends on in-depth studies of animal models that mimic the characteristics of clinical pathological pain. Currently, the commonly used models for the study of pathological pain mechanisms are formalin test models. Complete Freund's adjuvant model, partial sciatic nerve ligation model and sciatic nerve chronic compression model, etc. Up to now, new pathological pain models are still under development and exploration, the reason is that these animal pain models have their own characteristics. But also has its limitation, cannot completely simulate the pathological pain characteristic. In recent years, The research on the mechanism of pain information transmission and regulation by simulating pathological pain symptoms caused by animal toxin is increasing. In this study, we use the model of peripheral administration of animal toxin to explore the mechanism of pain sensitivity induced by animal toxin. The present study consists of the following two parts:. 1. The mechanism of pain sensitivity induced by intrasciatic injection of snake venom was observed by morphological and behavioral pharmacological methods. The results are as follows:. 1the demyelination of sciatic nerve was induced by intrasciatic nerve injection (SV). The most obvious changes of sciatic nerve myelin were observed 2 weeks after injection, but there was no obvious change in sciatic nerve in the control group treated with NS injection. 2 the expression of substance P, calcitonin gene-related peptide CGRPGAL1 and type 鈪

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