Department of Physical Therapy and Assistive Technology, National Yang Ming University, Taipei, Taiwan.
Microvasc Res. 2012 Mar;83(2):243-8. doi: 10.1016/j.mvr.2011.06.002. Epub 2011 Jun 23.
Impaired cutaneous blood flow and sweating dysfunction might be among the earliest manifestations of diabetic autonomic neuropathy. This study assessed the pathophysiological basis underlying skin vasomotion changes and their relation with progressive sudomotor dysfunction and other autonomic and somatic measures in subclinical diabetic feet. Laser Doppler skin perfusion was assessed on 68 diabetic and 25 control subjects. The low-frequency vasomotion was transformed into three frequency intervals 0.0095-0.021, 0.021-0.052 and 0.052-0.145 Hz, respectively, for the investigation of endothelial, neurogenic and myogenic effects on microcirculatory alterations. The diabetic patients were categorized into three groups by increasing severity of sudomotor dysfunction: SSR+ (sympathetic skin response present; 27 patients), SSR- (SSR absent; 23 patients) and at-risk (SSR absent and of preulcerative cracked skin; 18 patients). All diabetic patients underwent nerve conduction and cardiovascular autonomic studies. The total spectral and endothelial activity was significantly decreased only in the at-risk group. The SSR- group had lower neurogenic vasomotion than the SSR+ group (p<0.05). Although no statistical difference was noted between any group in absolute myogenic spectrum, the SSR- group had higher normalized myogenic activity than the SSR+ group (p<0.01). The larger drop in orthostatic pressure was paralleled by a reduction in the myogenic amplitude (r=-0.33, p<0.01). These results suggested that early impairment of low-frequency flow motion correlated closely with the presence of sudomotor dysfunction of subclinical feet mainly in neurogenic and endothelial components. Impaired systemic vascular tone as manifested by orthostatic hypotension was proportional to the degree of myogenic dysregulation in diabetic patients.
皮肤血流和出汗功能障碍可能是糖尿病自主神经病变的最早表现之一。本研究评估了亚临床糖尿病足中皮肤血管运动变化的病理生理基础及其与进行性出汗功能障碍以及其他自主和躯体测量的关系。在 68 例糖尿病患者和 25 例对照者中评估了激光多普勒皮肤灌注。低频血管运动分别转化为三个频率间隔 0.0095-0.021、0.021-0.052 和 0.052-0.145 Hz，以研究内皮、神经和肌源性因素对微循环变化的影响。根据出汗功能障碍的严重程度，将糖尿病患者分为三组：SSR+（存在交感神经皮肤反应；27 例）、SSR-（SSR 缺失；23 例）和高危（SSR 缺失和溃疡前干裂皮肤；18 例）。所有糖尿病患者均接受神经传导和心血管自主神经研究。仅在高危组中，总频谱和内皮活性显著降低。SSR-组的神经源性血管运动较 SSR+组降低（p<0.05）。尽管在任何一组之间，绝对肌源性频谱均无统计学差异，但 SSR-组的归一化肌源性活性高于 SSR+组（p<0.01）。直立位血压下降越大，肌源性幅度减小（r=-0.33，p<0.01）。这些结果表明，低频血流运动的早期损伤与亚临床足部出汗功能障碍的存在密切相关，主要涉及神经源性和内皮成分。体位性低血压表现出的全身血管张力受损与糖尿病患者肌源性失调的程度成正比。
