【摘要】： 背景與目的:外周組織損傷所致炎癥既伴隨有疼痛的產(chǎn)生(持續(xù)性自發(fā)痛、痛覺過敏等)同時(shí)又有明顯的紅、腫、熱的炎癥反應(yīng)。從炎癥反應(yīng)的原因和過程來看,它可進(jìn)一步分為神經(jīng)源性和組織源性兩種來源。神經(jīng)源性炎癥是指損傷后傷害性沖動(dòng)在向脊髓傳遞的過程中,沖動(dòng)又經(jīng)軸索反射(axon reflex)和/或背根反射(dorsal root reflex)逆行傳遞到外周神經(jīng)終末,導(dǎo)致P物質(zhì)(substance P, SP)及降鈣素相關(guān)基因肽(calcitonin gene-related peptide, CGRP)等活性物質(zhì)的釋放,擴(kuò)張外周血管,促進(jìn)炎癥的發(fā)生。組織源性炎癥主要指局部損傷導(dǎo)致大量的炎性物質(zhì)釋放(如緩激肽、PGE2、5-HT、組胺及細(xì)胞激肽等),導(dǎo)致炎癥的發(fā)生。 周圍組織炎癥所引起的痛覺過敏依賴脊髓背根神經(jīng)元的興奮性增加和初級(jí)傳入傷害性感受器的敏化。傷害性刺激導(dǎo)致的神經(jīng)遞質(zhì)的釋放能夠增加細(xì)胞內(nèi)Ca2+濃度,Ca2+濃度的增加又促進(jìn)鈣離子依賴的蛋白激酶C(protein kinase C, PKC)的激活。PKC作為一種蛋白激酶能夠影響突觸傳遞的整個(gè)順序,包括神經(jīng)遞質(zhì)釋放、受體敏感性、長時(shí)程增強(qiáng)以及離子通道活性。在前列腺素誘致的大鼠炎癥模型中表明,蛋白激酶A(protein kinase A, PKA)同樣也參與初級(jí)傳入神經(jīng)元的敏化,而且還可能與脊髓水平的傷害性疼痛過程有關(guān)。 越來越多的證據(jù)表明cAMP-PKA和二脂酰甘油(diacylglycerol, DAG)-PKC途徑在傷害性疼痛的傳遞過程中起到重要的作用。目前關(guān)
[Abstract]:Background & AIM: inflammation caused by peripheral tissue injury is accompanied by pain (persistent spontaneous pain, hyperalgesia, etc.) but also has obvious inflammation reaction of red, swelling and heat. According to the cause and process of inflammatory reaction, it can be further divided into two sources: neurogenic and tissue-derived. Neurogenic inflammation refers to the retrograde transmission of nociceptive impulses to peripheral nerve terminals through axonal reflex (axon reflex) and / or dorsal root reflex (dorsal root reflex) during the transmission of nociceptive impulses to the spinal cord after injury, resulting in substance P (substance P,. SP and calcitonin related gene peptide (calcitonin gene-related peptide, CGRP) release, dilate peripheral blood vessels and promote inflammation. Tissue-derived inflammation mainly refers to the local injury leading to the release of a large number of inflammatory substances (such as bradykinin, PGE2,5-HT, histamine and cell kinin), leading to inflammation. Hyperalgesia induced by peripheral inflammation depends on increased excitability of spinal dorsal root neurons and sensitization of primary afferent nociceptive receptors. The release of neurotransmitters induced by nociceptive stimulation can increase intracellular Ca2 concentration, while the increase of Ca2 concentration promotes calcium-dependent protein kinase C (protein kinase C,. PKC, as a protein kinase, can affect the entire sequence of synaptic transmission, including neurotransmitter release, receptor sensitivity, long term enhancement and ion channel activity. In the rat inflammatory model induced by prostaglandin, protein kinase A (protein kinase A, PKA) is also involved in the sensitization of primary afferent neurons and may be related to nociceptive pain at the spinal cord level. There is growing evidence that cAMP-PKA and diglyceride (diacylglycerol, DAG)-PKC pathways play an important role in the transmission of nociceptive pain. Current level
【學(xué)位授予單位】：大連醫(yī)科大學(xué)
【學(xué)位級(jí)別】：碩士
【學(xué)位授予年份】：2006
【分類號(hào)】：R363

【共引文獻(xiàn)】

相關(guān)博士學(xué)位論文 前2條

1 袁維秀;氯胺酮治療慢性神經(jīng)源性疼痛作用機(jī)制的實(shí)驗(yàn)研究[D];中國人民解放軍軍醫(yī)進(jìn)修學(xué)院;2004年

2 李連濤;潛在激痛點(diǎn)高敏感性的機(jī)制研究[D];山東大學(xué);2008年

相關(guān)碩士學(xué)位論文 前3條

1 戴飛紅;rSNSR1和5-HT_（2A）受體調(diào)節(jié)傷害性感受的細(xì)胞學(xué)基礎(chǔ)[D];福建師范大學(xué);2010年

2 吳樂;腺苷抑制大鼠脊髓背角淺層神經(jīng)元的GABA反應(yīng)[D];中國人民解放軍第四軍醫(yī)大學(xué);2003年

3 蔡巧燕;外周組織5-羥色胺2A受體在角叉菜膠誘發(fā)的炎性痛維持過程中的作用機(jī)制[D];福建師范大學(xué);2008年

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本文編號(hào)：2353017