Kindgen-Milles D, Arndt J O
Institute of Experimental Anesthesiology, Heinrich-Heine University Düsseldorf, Moorenstr. 5, D-40225 Düsseldorf, Germany.
Pain. 1996 Jan;64(1):139-142. doi: 10.1016/0304-3959(95)00081-X.
In humans, both nitric oxide (NO) and bradykinin, a naturally occurring algetic and a potent NO liberator, evoke pain from hand veins. The afferent innervation of these veins consists solely of polymodal nociceptors which are located close to the endothelium, a well-known source of NO, thus suggesting NO as a chemical link in nociception. Consistent with this hypothesis, our observations show that neither bradykinin, nor hyperosmolar solutions (a noxious physicochemical stimulus) evoke pain from hand vein segments that have been exposed to the NO-synthase (NOS) inhibitor NG-mono-methyl-L-arginine. An intact NOS pathway is therefore a prerequisite for pain to be evoked by bradykinin and hyperosmolar solutions from veins, indicating for the first time in humans that vascular pain is mediated by NO. Thus, new directions for research on analgesics may be opened.
在人类中，一氧化氮（NO）和缓激肽（一种天然存在的致痛物质且是一种强效的NO释放剂）都会引起手部静脉疼痛。这些静脉的传入神经支配仅由多模式伤害感受器组成，它们位于靠近内皮的位置，而内皮是众所周知的NO来源，因此提示NO是痛觉感受中的化学联系。与这一假设一致，我们的观察结果表明，缓激肽和高渗溶液（一种有害的物理化学刺激）都不会引起已暴露于一氧化氮合酶（NOS）抑制剂NG-单甲基-L-精氨酸的手部静脉段疼痛。因此，完整的NOS途径是缓激肽和高渗溶液从静脉引发疼痛的先决条件，这首次在人类中表明血管性疼痛是由NO介导的。因此，可能会开辟镇痛药研究的新方向。
