Yamamoto T, Shimoyama N
Department of Anesthesiology, School of Medicine, Chiba University, Japan.
Anesthesiology. 1995 May;82(5):1266-73. doi: 10.1097/00000542-199505000-00022.
Nitric oxide (NO) has been shown to be involved in mediating nociceptive information transmission in the spinal cord. It is known that the N-methyl-D-aspartate receptor plays an important role in the development of the spinal facilitation evoked by a protracted small afferent input and that this effect is mediated at least in part by NO. Recently, it has been found that N-methyl-D-aspartate receptor-mediated spinal facilitation is crucial in the development of thermal hyperesthesia evoked by a nerve constriction injury. In the current study, we investigated the role of NO in the development of thermal hyperesthesia after a nerve constriction injury.
The Bennett and Xie model (four loose chromic gut ligations around the rat sciatic nerve) was used to examine the development of thermal hyperesthesia. An NO synthase inhibitor (N omega-nitro-L-arginine or N omega-nitro-L-arginine methyl ester hydrochloride), rat hemoglobin, or L-arginine was administered intrathecally 10 min before the nerve injury (pretreatment study) or 15 min after the nerve injury (posttreatment study).
Pretreatment but not posttreatment administration of NO synthase inhibitor significantly delayed the development of thermal hyperesthesia. The effect of NO synthase inhibitor was reversed by the coadministration of L-arginine but not by the coadministration of D-arginine. Pretreatment with rat hemoglobin also delayed the development of thermal hyperesthesia. L-Arginine itself had no effect on the development of thermal hyperesthesia.
NO may play an important role in the development of N-methyl-D-aspartate receptor-mediated spinal facilitation after a nerve constriction injury.
一氧化氮（NO）已被证明参与介导脊髓中的伤害性信息传递。已知N-甲基-D-天冬氨酸受体在长时间的小传入输入诱发的脊髓易化发展中起重要作用，并且这种作用至少部分由NO介导。最近，已发现N-甲基-D-天冬氨酸受体介导的脊髓易化在神经压迫损伤诱发的热感觉过敏发展中起关键作用。在本研究中，我们研究了NO在神经压迫损伤后热感觉过敏发展中的作用。
使用Bennett和Xie模型（在大鼠坐骨神经周围进行四处松弛的铬肠线结扎）来检查热感觉过敏的发展。在神经损伤前10分钟（预处理研究）或神经损伤后15分钟（后处理研究）鞘内注射一氧化氮合酶抑制剂（Nω-硝基-L-精氨酸或盐酸Nω-硝基-L-精氨酸甲酯）、大鼠血红蛋白或L-精氨酸。
一氧化氮合酶抑制剂的预处理而非后处理显著延迟了热感觉过敏的发展。L-精氨酸共同给药可逆转一氧化氮合酶抑制剂的作用，而D-精氨酸共同给药则不能。大鼠血红蛋白预处理也延迟了热感觉过敏的发展。L-精氨酸本身对热感觉过敏的发展没有影响。
NO可能在神经压迫损伤后N-甲基-D-天冬氨酸受体介导的脊髓易化发展中起重要作用。
