Winkler T, Sharma H S, Stålberg E, Olsson Y
Department of Clinical Neurophysiology, University Hospital, Uppsala, Sweden.
Neuroscience. 1993 Feb;52(4):1057-67. doi: 10.1016/0306-4522(93)90552-q.
The potential efficacy of indomethacin (a potent inhibitor of endogenous prostaglandin synthesis) on spinal cord-evoked potentials and edema formation occurring after a focal trauma to the spinal cord was examined in a rat model. The spinal cord evoked potentials were recorded in urethane-anesthetized male rats using monopolar electrodes placed epidurally over the T9 (rostral) and T12 (caudal) segments after stimulation of the ipsilateral right tibial and sural nerves. Reference electrodes were placed in the corresponding paravertebral muscles. The spinal cord evoked potential consisted of a small positive peak followed by a broad and high negative peak. Amplitudes and latencies of the maximal positive peak and the maximal negative peak were measured. The latencies and amplitudes 30 min before injury were used as references (100%). A complete loss was denoted as 0%. All the potentials were quite stable during 30 min of recording before injury. Infliction of trauma to the T10-T11 segments of the spinal cord with a sterile scalpel blade (about 5 mm longitudinal and 2 mm deep incision into the right dorsal horn extending to Rexed's laminae VII) in untreated animals resulted in an immediate depression of the rostral maximal negative peak amplitude (60-100%) which persisted during 5 h of recording. The latencies of the rostral as well as caudal maximal negative and positive peaks increased successively from 2 h post-trauma. In this group of animals, 5 h after injury the spinal cord water content in the traumatized segments was increased by more than 6% as compared with a group of uninjured animals. Pretreatment with indomethacin (10 mg/kg body weight i.p. 30 min before injury) markedly attenuated the immediate decrease in the maximal negative peak amplitude after injury, but did not influence the successive latency increase. However, the increase in the water content of the traumatized cord after 5 h was less pronounced compared with untreated injured rats. Our results show a beneficial effect of indomethacin on trauma-induced spinal cord evoked potential changes and edema formation. Prostaglandins may thus influence early bioelectrical changes occurring in traumatized spinal cord not reported earlier. The findings support the view that early recording of spinal cord evoked potential may be useful to predict the outcome in some forms of spinal cord injuries.
在大鼠模型中，研究了吲哚美辛（一种内源性前列腺素合成的强效抑制剂）对脊髓局灶性创伤后脊髓诱发电位和水肿形成的潜在疗效。在乌拉坦麻醉的雄性大鼠中，使用硬膜外放置在T9（头端）和T12（尾端）节段上方的单极电极，在刺激同侧右胫神经和腓肠神经后记录脊髓诱发电位。参考电极置于相应的椎旁肌中。脊髓诱发电位由一个小的正峰和随后一个宽而高的负峰组成。测量最大正峰和最大负峰的振幅和潜伏期。损伤前30分钟的潜伏期和振幅用作参考（100%）。完全丧失记为0%。在损伤前记录的30分钟内，所有电位都相当稳定。在未治疗的动物中，用无菌手术刀刀片对脊髓T10 - T11节段造成创伤（在右背角纵向约5 mm、深2 mm切口，延伸至Rexed板层VII），导致头端最大负峰振幅立即降低（60 - 100%），在记录的5小时内持续存在。创伤后2小时起，头端以及尾端最大负峰和正峰的潜伏期相继增加。在这组动物中，与未受伤动物组相比，损伤后5小时创伤节段的脊髓含水量增加超过6%。吲哚美辛预处理（损伤前30分钟腹腔注射10 mg/kg体重）显著减轻了损伤后最大负峰振幅的立即下降，但不影响潜伏期的相继增加。然而，与未治疗的受伤大鼠相比，5小时后创伤脊髓的含水量增加不那么明显。我们的结果显示吲哚美辛对创伤诱导的脊髓诱发电位变化和水肿形成有有益作用。因此，前列腺素可能影响创伤脊髓中早期未报道的生物电变化。这些发现支持了早期记录脊髓诱发电位可能有助于预测某些形式脊髓损伤预后的观点。
