Holthusen H, Ding Z
Institut für Experimentelle Anaesthesiologie, Heinrich-Heine-Universität Düsseldorf, Germany.
Neurosci Lett. 1997 May 16;227(2):111-4. doi: 10.1016/s0304-3940(97)00314-5.
We tested the hypothesis that nitric oxide (NO) is involved in vascular nociception of physical stimuli in humans. Vascularly isolated hand vein segments of six healthy volunteers were pretreated with the NO synthase inhibitor, N(G)-nitro-L-arginine methyl ester (L-NAME; 10(-7)-10(-4) M) and repeatedly subjected to noxious thermal (2 degrees C, 52 degrees C) or mechanical stimuli (balloon distention) and, for control, to the endogenous algetic bradykinin (10(-6) M). L-NAME prevented in a concentration-related manner the algesic action of bradykinin, but had no effect on pain evoked by heat, cold, or stretch. NO is therefore not a general chemical link in nociception.
我们检验了一氧化氮（NO）参与人体物理刺激的血管伤害感受这一假说。对6名健康志愿者的离体手部静脉节段用一氧化氮合酶抑制剂N（G）-硝基-L-精氨酸甲酯（L-NAME；10（-7）-10（-4）M）进行预处理，然后反复施加有害热刺激（2℃、52℃）或机械刺激（球囊扩张），作为对照，施加内源性致痛物质缓激肽（10（-6）M）。L-NAME以浓度相关的方式阻断了缓激肽的致痛作用，但对热、冷或拉伸诱发的疼痛没有影响。因此，NO不是伤害感受中的一般化学联系。
