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咪达唑仑对兔脊髓背角神经元反应的抑制作用。

Suppressant effects of midazolam on responses of spinal dorsal horn neurones in rabbits.

作者信息

Miyamoto K, Wakita K, Okuda T, Fuji K, Suekane K

机构信息

Department of Anaesthesiology, Kinki University School of Medicine, Osaka Dental University, Japan.

出版信息

Neuropharmacology. 1992 Jan;31(1):49-53. doi: 10.1016/0028-3908(92)90160-q.

Abstract

Recordings of noxious intra-arterial bradykinin (BK)-induced chemonociceptive and spontaneous activity from 30 single spinal lamina V neurones of the dorsal horns in non-anaesthetized and decerebrated rabbits, were performed with tungsten microelectrodes. Intravenous injection of midazolam (0.2 mg/kg; 7 neurones) depressed BK-induced neural discharges by 55.0 +/- 6.2% (P less than 0.05) and 57.9 +/- 8.4% (P less than 0.05) 5 and 25 min after administration, respectively. Treatment with flumazenil (0.2 mg/kg, i.v.; 7 neurones), administered 20 min after midazolam, completely reversed the inhibition by midazolam of the BK-induced spinal lamina V neural responses and spontaneous neuronal activity. In contrast, a large dose of naloxone (1.0 mg/kg, i.v.; 6 neurones), administered 20 min after midazolam, failed to alter the midazolam-induced depressant effects on the nociceptive responses, at the spinal dorsal horn. Treatments with flumazenil (5 neurones) and naloxone (5 neurones) did not influence either the spontaneous or the BK-induced neuronal discharges, recorded in spinal lamina V cells. Midazolam depressed the nociceptive responses probably through its agonistic activity on the binding to the GABA-benzodiazepine-barbiturate system in the spinal dorsal horn.

摘要

采用钨微电极记录了30只未麻醉和去大脑家兔脊髓背角单个Ⅴ层神经元对动脉内注射有害缓激肽(BK)诱发的化学伤害性感受和自发活动。静脉注射咪达唑仑(0.2mg/kg;7个神经元)后5分钟和25分钟,分别使BK诱发的神经放电减少55.0±6.2%(P<0.05)和57.9±8.4%(P<0.05)。在咪达唑仑给药20分钟后静脉注射氟马西尼(0.2mg/kg;7个神经元),可完全逆转咪达唑仑对BK诱发的脊髓Ⅴ层神经反应和自发神经元活动的抑制作用。相比之下,在咪达唑仑给药20分钟后静脉注射大剂量纳洛酮(1.0mg/kg;6个神经元),未能改变咪达唑仑对脊髓背角伤害性反应的抑制作用。氟马西尼(5个神经元)和纳洛酮(5个神经元)处理对脊髓Ⅴ层细胞记录的自发或BK诱发的神经元放电均无影响。咪达唑仑可能通过其对脊髓背角γ-氨基丁酸-苯二氮䓬-巴比妥酸盐系统结合位点的激动活性来抑制伤害性反应。

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