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[阿片类药物引起的瘙痒。机制与治疗方案]

[Opioid-induced pruritus. Mechanisms and treatment regimens].

作者信息

Schmelz M

机构信息

Institut für Anästhesiologie und Operative Intensivmedizin, Klinische Fakultät Mannheim, Ruprecht-Karls-Universität Heidelberg, Theodor-Kutzer-Ufer 1-3, 68135 Mannheim, Deutschland.

出版信息

Anaesthesist. 2009 Jan;58(1):61-5. doi: 10.1007/s00101-008-1478-8.

Abstract

Substantial progress has been achieved in recent years in research on the interaction between pain and pruritus. Over and above the known inhibition of pruritus by painful stimuli (e.g. scratching), a foundation for the explanation of opioid-induced pruritus was laid through the discovery of pruritus-specific neuronal processing channels. Although traditionally the degranulating effect of opioids on mast cells was assumed to be the essential mechanism, it is now clear that opioids can also induce itching at the spinal level. Neurons of the dorsal horn of the pain system inhibit spinal itch neurons. If this inhibition is weakened by opioids, the disinhibited itch neurons become active and mediate itching, without stimulation of the primary afferent peripheral nerves. Spinal triggering of itching is observed in particular by activation of mu-opioid receptors (mu-OR), while kappa-OR surprisingly suppress itch. The therapeutic implications of this interaction will be described.

摘要

近年来,疼痛与瘙痒相互作用的研究取得了重大进展。除了已知的疼痛刺激(如搔抓)对瘙痒的抑制作用外,瘙痒特异性神经元处理通道的发现为解释阿片类药物引起的瘙痒奠定了基础。虽然传统上认为阿片类药物对肥大细胞的脱颗粒作用是其主要机制,但现在很清楚,阿片类药物也可在脊髓水平诱发瘙痒。疼痛系统背角的神经元抑制脊髓瘙痒神经元。如果这种抑制因阿片类药物而减弱,去抑制的瘙痒神经元就会变得活跃并介导瘙痒,而无需刺激初级传入外周神经。特别是通过激活μ-阿片受体(mu-OR)可观察到脊髓引发的瘙痒,而κ-OR却出人意料地抑制瘙痒。将描述这种相互作用的治疗意义。

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