链脲佐菌素诱导的糖尿病大鼠的机械性痛觉过敏并非由交感神经维持。

Mechanical hyperalgesia in streptozotocin-diabetic rats is not sympathetically maintained.

作者信息

Ahlgren S C, Levine J D

机构信息

Department of Anatomy, University of California, San Francisco 94143-0452.

出版信息

Brain Res. 1993 Jul 9;616(1-2):171-5. doi: 10.1016/0006-8993(93)90206-3.

DOI:10.1016/0006-8993(93)90206-3

PMID:8358610

Abstract

It has been suggested that the mechanism underlying the pain that occurs in patients with diabetic neuropathy may be similar to that mediating sympathetically maintained pain (SMP), such as occurs in patients with reflex sympathetic dystrophy. To evaluate this suggestion we have examined a model of diabetes mellitus, the streptozotocin-diabetic (STZ-D) rat, for features characteristic of SMP. We demonstrate that the decrease in nociceptive threshold observed in the STZ-D rat is not attenuated by chemical sympathectomy nor exacerbated by intradermal injection of norepinephrine (NE). In addition, the NE content is markedly decreased in the skin of the STZ-D rat. These results suggest that altered nociceptive thresholds associated with diabetic neuropathy are not sympathetically maintained.

摘要

有人提出，糖尿病性神经病变患者所出现疼痛的潜在机制可能与介导交感神经维持性疼痛（SMP）的机制相似，比如反射性交感神经营养不良患者所出现的疼痛。为了评估这一观点，我们研究了糖尿病模型——链脲佐菌素诱导的糖尿病（STZ-D）大鼠，以寻找SMP的特征。我们发现，STZ-D大鼠中观察到的伤害性感受阈值降低，并不会因化学性交感神经切除术而减弱，也不会因皮内注射去甲肾上腺素（NE）而加剧。此外，STZ-D大鼠皮肤中的NE含量显著降低。这些结果表明，与糖尿病性神经病变相关的伤害性感受阈值改变并非由交感神经维持。