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目的：多数关于ＮＯ对痛觉调制的报道，认为ＮＯ在脑内有痛敏作用。本工作研究ＮＯ在脊髓中的作用。方法：由于ＮＯ的半衰期很短，因此本工作采用给动物脊髓蛛网膜下腔注射（ｉｔｈ）ＮＯ的前体，精氨酸、精精二肽和在体内自发释放ＮＯ的硝普钠（ＳＮＰ）以及ＮＯ合成酶（ＮＯＳ）抑制剂ＮＧ硝基Ｌ精氨酸（ＮＮＬＡ），借以调制脊髓中ＮＯ的释放，并用大鼠幅射热甩尾实验观察脊髓中ＮＯ对大鼠痛阈的影响。结果：ｉｔｈ不同剂量（１０μｇ、２０μｇ、４０μｇ）的Ｌ精氨酸、精精二肽以及三种剂量（１．０μｇ、２．０μｇ、４．０μｇ）的ＳＮＰ，均引起明显的痛敏效应，并在该剂量范围内呈量效关系。三种剂量的精精二肽的痛敏作用，要比Ｌ精氨酸的痛敏作用强，并持续更长的时间。ｉｔｈ三种剂量（２．５μｇ、５μｇ、１０μｇ）的ＮＯＳ抑制剂ＮＮＬＡ则具有明显的镇痛作用，镇痛可持续２０ｍｉｎ以上，并呈剂量效应关系。结论：提高脊髓中ＮＯ水平具有痛敏作用，降低脊髓中ＮＯ水平具有镇痛作用。
Aim: Most reports of NO on pain modulation suggest that NO has pain-sensitivity effects in the brain. This work to study the role of NO in the spinal cord. Methods: Because of the short half-life of NO, this study used injection of ith precursors, arginine and sperm-dipeptide into the subarachnoid space of animals and spontaneously released nitric oxide (SNP) ) And NO synthase (NOS) inhibitor NG-nitro-L-arginine (NNLA) to modulate the release of NO from the spinal cord. Impact. Results: L-arginine, refined-refined dipeptide and three SNPs (1.0μg, 2.0μg, 4.0μg) at different doses (10μg, 20μg, 40μg) Effect, and in the dose range was dose-effect relationship. Three doses of fine-refined dipeptide pain-sensitive effect than the L-arginine pain-sensitive effect, and lasts longer. ith three doses (2.5μg, 5μg, 10μg) of NOS inhibitor NNLA has a significant analgesic effect, analgesia sustainable 20min or more, and the dose-response relationship. Conclusion: Increasing the level of NO in spinal cord has the effect of relieving pain and reducing the level of NO in spinal cord.