BLOOD-FLOW PATTERNS IN PAINFUL DIABETIC NEUROPATHY
BLOOD-FLOW PATTERNS IN PAINFUL DIABETIC NEUROPATHY
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DOI：
10.1007/bf00276968
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发表时间：
1984-01-01
期刊：
影响因子：
8.2
通讯作者：
WATKINS, PJ
中科院分区：
文献类型：
--
作者：
ARCHER, AG;ROBERTS, VC;WATKINS, PJ
伴有神经病变的糖尿病患者外周血流量定性增加。使用非侵入性水银应变计体积描记术和多普勒超声描记术技术测量患有神经病的糖尿病患者的足部中的实际血流量;在20 ℃的环境温度下，其平均比正常增加5倍。22.degree. C.在严重疼痛性神经病变患者中，交感神经唤醒刺激可减少这种高流量，而在严重非疼痛性感觉神经病变患者中，交感神经唤醒刺激无法逆转这种高流量。血流量的减少与神经性疼痛的减少有关。22例糖尿病患者严重的感觉神经病变和8痛性神经病变进行了研究。两组神经病变患者的静息足血流量均较高。严重感觉神经病变患者的大脚趾血流为29.3 ± 0.001。9.2 ml. cntdot. min-1. 100 ml-1（平均值±. SD）和疼痛性神经病变组，25.9 ±。7.5，而5.2 . ±-。2.4 ml. cntdot. min-1.非糖尿病对照组100 ml-1（P < 0.001）。高足部皮肤温度也记录在神经病变组中，反映了高血流量。疼痛性神经病患者保留了对唤醒刺激做出反应的收缩外周血管的能力，并且与感觉性神经病患者相比，外周血流平均减少了32%，而感觉性神经病患者的反应平均仅为10%。周围交感神经缺陷，负责高血流量和潜在的逆转，这种流动在疼痛性神经病变的证明可能是重要的，在进一步了解这种疼痛的病因和治疗。
Peripheral blood flow is qualitatively increased in diabetic patients with neuropathy. The actual blood flow in the feet of diabetic patients with neuropathy was measured using noninvasive mercury strain gauge plethysmography and Doppler sonogram techniques; it is increased on average 5 times above normal at an ambient temperature of 20.degree.-22.degree. C. Reduction of this high flow by sympathetic arousal stimuli proved possible in those with severe painful neuropathy contrasting strongly with failure to reverse it in those with severe nonpainful sensory neuropathy. Reduction of blood flow was associated with reduction in neuropathic pain. Twenty-two diabetic patients with severe sensory neuropathy and 8 with painful neuropathy were studied. High resting foot blood flows were demonstrated in both groups with neuropathy. The big toe flow in those with severe sensory neuropathy was 29.3 .+-. 9.2 ml .cntdot. min-1 .cntdot. 100 ml-1 (mean .+-. SD) and in the painful neuropathy group, 25.9 .+-. 7.5, compared with 5.2 .+-. 2.4 ml .cntdot. min-1 .cntdot. 100 ml-1 in the nondiabetic control subjects (P < 0.001). High foot skin temperatures also were recorded in the groups with neuropathy, reflecting the high blood flow. The subjects with painful neuropathy retained the ability to constrict peripheral blood vessels in response to arousal stimuli, and reduce peripheral flow on average by 32% compared with the patients with sensory neuropathy who responded on average by only 10%. The demonstration of a peripheral sympathetic defect, responsible for the high blood flow and the potential reversal of such flow in painful neuropathy may be important in the further understanding of the etiology of such pain and its treatment.