Antognini Joseph F, Atherley Richard J, Dutton Robert C, Laster Michael J, Eger Edmond I, Carstens Earl
Department of Anesthesiology and Pain Medicine, University of California, Davis, California 95616, USA.
Anesth Analg. 2007 Apr;104(4):829-35. doi: 10.1213/01.ane.0000255696.11833.24.
Because of the logistical obstacles to measurement under hyperbaric conditions, the effect of nitrous oxide (N2O) alone on spinal neuronal responses has not been tested. We hypothesized that, like other inhaled anesthetics, N2O would depress spinal neuronal responses to noxious stimulation.
The lumbar spinal cord was exposed in rats anesthetized with isoflurane. Mechanically ventilated rats were placed into a hyperbaric chamber and needle electrodes were inserted into the hindpaws. Isoflurane administration was discontinued and anesthesia converted to N2O by pressurizing the chamber with N2O. A microelectrode was inserted into the lumbar cord using computer-controlled motors and a hydraulic microdrive. Neuronal responses to electrical stimulation of the hindpaw were sought at 1.5, 2, and 2.5 atm N2O (0.8-1.3 minimum alveolar concentration).
Increasing N2O partial pressures variably affected neuronal responses to a 2 s 100-Hz electrical stimulus. Neuronal depth and neuronal response were correlated, with superficial neurons tending to be facilitated, while deeper neurons were depressed; (overall responses were 1331 +/- 408, 1594 +/- 383, and 1578 +/- 500 impulses/min at 1.5, 2, and 2.5 atm N2O, respectively; mean, standard error). N2O did not affect neuronal responses to a repetitive "windup" stimulus. Infusion of the N-methyl-d-aspartate blocker MK-801 into separate rats increased the neuronal response to the 100-Hz stimulus (from 781 +/- 216 to 1352 +/- 269 impulses/min, P < 0.05).
N2O facilitated superficial spinal neuronal responses to noxious stimulation while depressing deeper neurons. These results suggest that anesthetic partial pressures of N2O have divergent effects on spinal neuronal responses to noxious stimulation, the specific responses depending on the depth of the spinal neurons.
由于在高压条件下进行测量存在后勤障碍,一氧化二氮(N2O)单独对脊髓神经元反应的影响尚未得到测试。我们假设,与其他吸入性麻醉剂一样,N2O会抑制脊髓神经元对有害刺激的反应。
在异氟烷麻醉的大鼠中暴露腰脊髓。将机械通气的大鼠放入高压舱中,并将针电极插入后爪。停止给予异氟烷,通过用N2O对舱室加压将麻醉转换为N2O。使用计算机控制的电机和液压微驱动器将微电极插入腰脊髓。在1.5、2和2.5个大气压的N2O(0.8 - 1.3最低肺泡浓度)下寻找神经元对后爪电刺激反应。
增加N2O分压对神经元对2秒100赫兹电刺激的反应有不同影响。神经元深度与神经元反应相关,浅层神经元倾向于易化,而深层神经元被抑制;(在1.5、2和2.5个大气压的N2O下,总体反应分别为1331±408、1594±383和1578±500次冲动/分钟;平均值,标准误差)。N2O不影响神经元对重复性“windup”刺激的反应。向单独的大鼠输注N - 甲基 - d - 天冬氨酸阻滞剂MK - 801增加了神经元对100赫兹刺激的反应(从781±216增加到1352±269次冲动/分钟,P < 0.05)。
N2O促进脊髓浅层神经元对有害刺激的反应,同时抑制深层神经元。这些结果表明,N2O的麻醉分压对脊髓神经元对有害刺激的反应有不同影响,但具体反应取决于脊髓神经元的深度。