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本文探讨耗竭脊髓背角P物质(Substance P,SP)对外周神经损伤所引起的痛觉过敏的影响,结果表明给新生大鼠皮下注射SP抗血清,成年后脊髓背角SP明显耗竭(SP含量下降48.9％)的动物对损伤坐骨神经所造成的痛觉过敏较注射正常兔血清的对照组明显减轻(P<0.05),且背角SP含量越低,痛觉过敏表现也越轻。此外,还对SP参与调节外周神经损伤性痛觉过敏的机制进行了讨论。
This study was designed to investigate the effect of substance P (SP) on hyperalgesia induced by peripheral nerve injury in spinal cord. The SP antiserum was injected subcutaneously into neonatal rats and the spinal dorsal horn SP was significantly depleted (SP content decreased 48.9%) had less hyperalgesia than the control group injected with normal rabbit serum (P <0.05), and the lower the SP content of the dorsal horn, the less hyperalgesia. In addition, the mechanism of SP involved in the regulation of peripheral nociceptive hyperalgesia is also discussed.