Lui P W, Chang G J, Lee T Y, Chan S H
Department of Anesthesiology, National Yang-Ming Medical College, Taipei, Taiwan, ROC.
Neurosci Lett. 1993 Jul 23;157(2):145-8. doi: 10.1016/0304-3940(93)90723-x.
The present study examined the effect of denervating the coerulospinal noradrenergic pathway on the muscular rigidity elicited by fentanyl in Sprague-Dawley rats anesthetized with ketamine. We demonstrated that the dopamine-beta-hydroxylase-positive nerve terminals arborizing on spinal motoneurons that innervate the sacrococcygeus dorsi lateralis (SCDL) muscle were significantly eliminated by DSP4 treatment. Unilateral microinjection of fentanyl (2.5 micrograms/50 nl) into the locus coeruleus of these animals also failed to evoke discernible increase in the electromyographic activity recorded from the SCDL muscle. These results lend further support for our previous finding that the coerulospinal noradrenergic neurotransmission is critically involved in fentanyl-induced muscular rigidity.
本研究检测了去甲肾上腺素能蓝斑脊髓通路失神经支配对氯胺酮麻醉的Sprague-Dawley大鼠中芬太尼诱发的肌肉强直的影响。我们证明,DSP4处理可显著消除支配骶尾背外侧肌(SCDL)的脊髓运动神经元上的多巴胺-β-羟化酶阳性神经终末分支。对这些动物的蓝斑进行单侧微量注射芬太尼(2.5微克/50纳升),也未能引起SCDL肌肉记录到的肌电图活动出现明显增加。这些结果进一步支持了我们之前的发现,即蓝斑脊髓去甲肾上腺素能神经传递在芬太尼诱发的肌肉强直中起关键作用。