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鞘内注射吗啡的镇痛作用在大鼠脊髓中上行伤害性活动中得到证实,同时证明了蛙皮素和胆囊收缩素八肽无效。

Analgesic effect of intrathecal morphine demonstrated in ascending nociceptive activity in the rat spinal cord an in effectiveness of caerulein and cholecystokinin octapeptide.

作者信息

Doi T, Jurna I

出版信息

Brain Res. 1982 Feb 25;234(2):399-407. doi: 10.1016/0006-8993(82)90879-4.

Abstract

The effect of intrathecal injections of morphine and the two peptides, caerulein and cholecystokinin octapeptide (CCK-8), on the activity in ascending axons of the spinal cord evoked by electrical stimulation of primary nociceptive afferents was studied in spinal rats with decerebration. Morphine (20 microgram) depressed the spontaneous activity and the activity evoked from either A delta-or C-fibres. The co-activation by A delta-fibre stimulation of ascending axons activated by stimulation of C-fibres and the activity in ascending axons activated by stimulation of afferent A beta-fibres were not influenced by morphine. C-Fibre-evoked ascending activity was also depressed by morphine (10 microgram and 5 microgram). Ascending nociceptive activity was not changed by caerulein (30 ng) and CCK-8 300 ng, but it was depressed by a subsequent injection of morphine (20 microgram). The depressant effects of morphine were abolished by an intravenous injection of concluded that: (i) an intrathecal injection of morphine selectively depressed the ascending nociceptive activity; (ii) the depression produced by morphine is an equivalent for spinal analgesia following intrathecal injection of morphine to man; and (iii) the two components of the spinal nociceptive system, the motor and the sensory path, can independently be influenced by drugs.

摘要

在去大脑的脊髓大鼠中,研究了鞘内注射吗啡以及两种肽(蛙皮素和八肽胆囊收缩素(CCK - 8))对初级伤害性传入纤维电刺激诱发的脊髓上升轴突活动的影响。吗啡(20微克)抑制了自发活动以及由Aδ纤维或C纤维诱发的活动。Aδ纤维刺激对由C纤维刺激激活的上升轴突的共同激活以及由传入Aβ纤维刺激激活的上升轴突的活动不受吗啡影响。C纤维诱发的上升活动也被吗啡(10微克和5微克)抑制。蛙皮素(30纳克)和CCK - 8(300纳克)未改变上升性伤害性活动,但随后注射吗啡(20微克)则使其受到抑制。静脉注射纳洛酮可消除吗啡的抑制作用。得出以下结论:(i)鞘内注射吗啡选择性地抑制上升性伤害性活动;(ii)吗啡产生的抑制作用等同于鞘内注射吗啡对人体产生脊髓镇痛作用;(iii)脊髓伤害性系统的两个组成部分,运动和感觉路径,可被药物独立影响。

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