Yamamoto T, Shimoyama N, Mizuguchi T
Department of Anesthesiology, Chiba University, School of Medicine, Japan.
Anesthesiology. 1993 Nov;79(5):993-1002; discussion 28A. doi: 10.1097/00000542-199311000-00018.
Usually, a barrage of impulses ("injury discharge") is evoked following sensory nerve damage. It has been suggested that injury discharge may produce the hyperexcitatory state in the spinal cord, and this hyperexcitability may cause neurogenic pain. In the present study, the authors examined the role of injury discharge in developing the hyperesthetic state following nerve constriction injury.
A model of thermal hyperesthesia caused by a constriction injury created by making four loose ligations around the rat sciatic nerve was examined. To block the injury discharge, 0.5% bupivacaine was applied to the sciatic nerve before constriction injury. To block the hyperexcitatory state, (+)-MK-801, an N-methyl-D-aspartate antagonist, was administered intrathecally 15 min before the nerve lesion.
Blocking injury discharge significantly delayed the development of hyperesthesia. Bupivacaine had no effect on the development of hyperesthesia when bupivacaine was applied to the sciatic nerve 15 min after the nerve constriction injury. Systemic bupivacaine had no effect on the development of thermal hyperesthesia. Intrathecal (+)-MK-801 also delayed the development of hyperesthesia when (+)-MK-801 was administered intrathecally 15 min before the nerve injury. When (+)-MK-801 was administered 15 min after the nerve injury, (+)-MK-801 had no effect on the development of hyperesthesia.
These results suggest that injury discharge may induce facilitation of spinal dorsal horn neurons, and this spinal facilitation may play an important role in developing thermal hyperesthesia following sciatic nerve constriction injury.
通常，感觉神经损伤后会引发一连串的冲动（“损伤放电”）。有人提出，损伤放电可能会在脊髓中产生过度兴奋状态，而这种过度兴奋可能会导致神经源性疼痛。在本研究中，作者研究了损伤放电在神经压迫损伤后引发感觉过敏状态中的作用。
研究了通过在大鼠坐骨神经周围进行四处宽松结扎造成的压迫损伤所引起的热感觉过敏模型。为了阻断损伤放电，在压迫损伤前将0.5%布比卡因应用于坐骨神经。为了阻断过度兴奋状态，在神经损伤前15分钟鞘内注射N-甲基-D-天冬氨酸拮抗剂（+）-MK-801。
阻断损伤放电显著延迟了感觉过敏的发展。当在神经压迫损伤后15分钟将布比卡因应用于坐骨神经时，布比卡因对感觉过敏的发展没有影响。全身应用布比卡因对热感觉过敏的发展没有影响。当在神经损伤前15分钟鞘内注射（+）-MK-801时，鞘内注射（+）-MK-801也延迟了感觉过敏的发展。当在神经损伤后15分钟给予（+）-MK-801时，（+）-MK-801对感觉过敏的发展没有影响。
这些结果表明，损伤放电可能诱导脊髓背角神经元的易化，而这种脊髓易化可能在坐骨神经压迫损伤后引发热感觉过敏中起重要作用。
