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本文采用测量大鼠脚掌直径和后肢屈肌反射潜伏期以及Northernblot检测脊髓强啡肽mRNA的方法，研究了炎症反应-痛觉过敏-脊髓强啡肽mRNA表达的相关关系。发现将不同剂量的CFA注入大鼠一侧后脚掌后，该侧后脚掌即发生不同程度的炎症反应和痛觉过敏，二者之间呈正相关关系；同侧脊髓强啡肽mRNA表达增强，并与炎症反应和痛觉过敏均呈正相关关系。在注射不同剂量CFA诱发组织炎症反应、出现痛觉过敏和增加脊髓强啡肽mRNA表达时，似乎存在一个引发这些变化出现“跃变”的剂量。这些结果提示，持续的伤害性信息在脊髓水平的传递不是一个被动过程，而是一个包括背角环路中强啡肽能活动增强的中枢可塑性主动过程，从而导致产生痛觉过敏或／和痛觉记忆。防止这种对伤害性信息的传递起易化作用的改变，有利于防止外周组织损伤如手术损伤引起的痛觉过敏。
In this paper, the relationship between inflammatory response-hyperalgesia and spinal dynorphin mRNA expression was studied by measuring the diameter of the paw and the latency of flexor reflex in the hind limbs and detecting the mRNA of spinal dynorphin by Northern blot. It was found that different doses of CFA were injected into the rat’s dorsum of the hind paw. The inflammation of the hind paw and hyperalgesia occurred at different degrees. The expression of dynorphin mRNA was increased in the ipsilateral spinal cord Inflammation and hyperalgesia were positively correlated. There appears to be a dose of “jump” that triggers these changes when injected with different doses of CFA to induce tissue inflammation, hyperalgesia, and spinal dynorphin mRNA expression. These results suggest that the transmission of persistent nociceptive information at the spinal cord level is not a passive process but rather a central pro-active process that involves increased activity of dynorphin in the dorsal horn circulation leading to hyperalgesia and / or allodynia . Preventing this change of facilitative effect on the transmission of nociceptive information is advantageous for preventing hyperalgesia caused by peripheral tissue damage such as surgical injury.