Kumeta Y, Murata K, Kitahata L M, Aoki M, Nishio Y, Collins J G
Department of Anesthesiology, Yale University School of Medicine, New Haven, Connecticut 06510.
Anesthesiology. 1988 Sep;69(3):371-6. doi: 10.1097/00000542-198809000-00014.
This study was designed to examine the influence of spinally administered fentanyl on the spontaneous and noxiously evoked activity of high threshold (HT) and wide dynamic range (WDR) neurons in the superficial layers (lamina I and II) of the dorsal horn of cats made decerebrate and in which the spinal cord had been transected. Single unit activity was recorded using extracellular microelectrode recording techniques. Neuronal activity was evoked by the presentation of noxious radiant heat (51 degrees C) to the cells' receptive fields on the hind paws. Evoked activity of WDR neurons was monitored, both before and after the spinal administration of either 10 micrograms (n = 9) or 25 micrograms (n = 10) of fentanyl. HT neurons were examined before and after either 25 micrograms (n = 7) or 50 micrograms (n = 7) of spinally administered fentanyl. In all cases 31 min after fentanyl administration naloxone (0.1 mg) was administered intravenously (iv), and its antagonistic effect on the fentanyl suppression was determined. All doses of fentanyl tested suppressed both spontaneous and evoked activity of both types of neurons. Within 30 minutes 10 and 25 micrograms of fentanyl reduced the mean evoked activity of WDR neurons to 61% and 19% of control values, respectively, and 25 and 50 micrograms of fentanyl reduced the mean evoked activity of HT neurons to 70% and 47% of control values, respectively. Naloxone reversed the suppression seen in all cells studied. The results of the present study demonstrate that HT neurons are significantly less suppressed by the spinal administration of fentanyl than WDR neurons located in the same superficial layers of the dorsal horn.(ABSTRACT TRUNCATED AT 250 WORDS)
本研究旨在探讨脊髓给予芬太尼对去大脑并脊髓横断猫的背角浅层(I层和II层)高阈值(HT)和广动力范围(WDR)神经元的自发活动及伤害性诱发活动的影响。采用细胞外微电极记录技术记录单个单位活动。通过对后爪细胞感受野施加伤害性辐射热(51摄氏度)诱发神经元活动。在脊髓给予10微克(n = 9)或25微克(n = 10)芬太尼之前和之后,监测WDR神经元的诱发活动。在脊髓给予25微克(n = 7)或50微克(n = 7)芬太尼之前和之后,检查HT神经元。在所有情况下,芬太尼给药后31分钟静脉注射纳洛酮(0.1毫克),并确定其对芬太尼抑制作用的拮抗效果。所有测试剂量的芬太尼均抑制了两种类型神经元的自发活动和诱发活动。在30分钟内,10微克和25微克芬太尼分别将WDR神经元的平均诱发活动降低至对照值的61%和19%,25微克和50微克芬太尼分别将HT神经元的平均诱发活动降低至对照值的70%和47%。纳洛酮逆转了所有研究细胞中观察到的抑制作用。本研究结果表明,与位于背角同一浅层的WDR神经元相比,脊髓给予芬太尼对HT神经元的抑制作用明显较小。(摘要截短于250字)