TRH对大鼠脊髓损伤后SCBF和SEP的影响

脊髓损伤（ＳＣＩ）后内源性阿片肽释放，并参与脊髓的继发损伤机制。ＴＲＨ可阻断阿片肽的自主神经效应，而不影响痛觉。本实验探讨大剂量ＴＲＨ（２ｍｇ／ｋｇ／ｈ）治疗对大鼠脊髓打击伤（Ａｌｌｅｎｓ法１０ｇｘ５ｃｍ）后脊髓血流量（ＳＣＢＦ）和脊髓诱发电位（ＳＥＰ）的影响。脊髓损伤后１ｈ，ＳＣＢＦ开始显著下降，持续至伤后２４ｈ，ＳＥＰ峰潜时呈进行性延长趋势；伤后即刻静脉注射ＴＲＨ（２ｍｇ／ｋｇ／ｈ，共５次），可使伤后即刻和２４ｈ的ＳＣＢＦ显著升高，并使伤后ＳＣＢＦ下降时间延迟３ｈ，同时ＳＥＰ峰潜时有不同程度改善。结果表明，ＴＲＨ对受伤脊髓早期有一定的防治作用，并具有一定的后发效应；同时也可促进脊髓的神经传导功能。本文亦对ＴＲＨ治疗ＳＣＩ的病理生物学机制进行了讨论。

Effects of TRH on spinal cord blood flow and spinal evoked potential in rats with spinal cord injury

The endogenous opioids are released after spinal cord injury(SCI), and contributed to the secondary pathophysiologic mechanism. Thyrotropin-releasing hormone(TRH)is a partial physiologic opiate antagonist that reverses the autonomic effect of opioids without altering analgesia. The purpose of the present study were to investigate the effects of TRH on posttrau matic spinal cord blood flow(SCBF)and spinal evoked potentials(SEP), at an optimal dose (2mg/kg/h). At lh after SCI, SCBF was decreased significautly and progressively by 27% to 50%, and continued to fall at 24h postinjury. SEP's peak latencies tended to be delayed progressively. Meanwhile, SEP's peak latencies were ameliorated to various degrees. The result showed that TRH may protect the injuried spinal cord by delaying the decrease of SCBF. It can also enhance the neural conduction of the spinal cord. The TRH pathophysiologic mechanisms on SCI were discussed.