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糖尿病性神经病变中的微血管异常。

Abnormal microvasculature in diabetic neuropathy.

作者信息

Ward J D

机构信息

Royal Hallamshire Hospital, Sheffield, UK.

出版信息

Eye (Lond). 1993;7 ( Pt 2):223-6. doi: 10.1038/eye.1993.53.

Abstract

Microvascular abnormalities are prominent in the retina and kidney in diabetic subjects with the specific complications of the disease. It would not therefore be surprising to find similar changes in nerve, the other tissue prominently damaged in diabetes. A variety of biochemical abnormalities have been postulated as a cause of nerve damage but so far none has been reversed with any benefit to patients. It is now very clear that major structural and functional changes in the microvasculature occur in diabetic neuropathy and are probably involved in resulting nerve damage. Endothelial thickening of the endothelial basement membrane occurs, as does luminal occlusion caused by endothelial cell proliferation; human sural nerve is hypoxic; sural nerve epineurial arterioles are attenuated and involved in arteriovenous shunting associated with gross distension and tortuosity of veins; flow of fluorescein is impaired in neuropathic nerves and nerve conduction increment on exercise is impaired in neuropathy. Therapeutic intervention should now be directed at these gross abnormalities.

摘要

在患有糖尿病特定并发症的受试者中,视网膜和肾脏的微血管异常非常突出。因此,在糖尿病中另一个明显受损的组织——神经中发现类似变化也就不足为奇了。人们推测了多种生化异常作为神经损伤的原因,但迄今为止,没有任何一种能够逆转并给患者带来益处。现在很清楚的是,糖尿病性神经病变中微血管会发生主要的结构和功能变化,并且可能与由此导致的神经损伤有关。内皮基底膜增厚,内皮细胞增殖导致管腔闭塞;人腓肠神经缺氧;腓肠神经外膜小动脉变细,并参与与静脉明显扩张和迂曲相关的动静脉分流;荧光素在神经病变神经中的流动受损,神经病变中运动时神经传导增加也受损。现在治疗干预应针对这些明显的异常情况。

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