Woodman Richard J, Playford David A, Watts Gerald F
School of Public Health, Curtin University of Technology, Perth, Australia.
Diabetes Res Clin Pract. 2006 Jan;71(1):59-67. doi: 10.1016/j.diabres.2005.05.008. Epub 2005 Jul 18.
We examined basal forearm microcirculatory blood flow (FBF) using venous occlusive strain-gauge plethysmography in 47 middle-aged men and women [55+/-1 years] with Type 2 diabetes and 15 age-matched healthy individuals [52+/-3 years], all receiving aspirin. Blood flow was also measured following infusion of N(G)-monomethyl-L-arginine into the brachial artery to inhibit basal NO release (FBF+L-NMMA). Acetylcholine (ACh) and sodium nitroprusside (SNP) were administered to assess endothelium-dependent and endothelium-independent functions. Compared with controls, diabetic subjects had significantly lower vasodilatory responses to ACh and SNP (p<0.05 for each). Basal FBF and FBF+L-NMMA were increased in diabetic subjects compared with controls (2.4+/-0.2 ml/100ml/min versus 1.7+/-0.2 ml/100ml/min, p=0.02 and 1.9+/-0.1 ml/100ml/min versus 1.2+0.1 ml/100ml/min, p=0.01, respectively) whereas the change in FBF following L-NMMA was greater in the controls (-27% versus -19%, p=0.05). Amongst the diabetic subjects, pulse pressure and HDL cholesterol were independent predictors of FBF (b=0.04+/-0.01, adjusted r2=0.21 and p=0.001, and b=3.3+/-1.2, adjusted r2=0.12 and p=0.007, respectively) and FBF+L-NMMA (b=0.03+/-0.01, adjusted r2=0.20, p=0.002 and b=2.1+/-0.9, adjusted r2=0.09 and p=0.02, respectively). Diastolic blood pressure predicted the change in FBF with L-NMMA (b=-1.02+/-0.32, adjusted r2=0.20 and p=0.003). Our findings suggest that well controlled T2DM patients have impaired agonist-mediated vasodilatation of the forearm resistance arteries that is associated with impaired basal release of nitric oxide but an increase in the release of non-NO vasodilators. The latter may be a compensatory response to increased arterial stiffness and may be facilitated by an effect of HDL.
我们使用静脉阻塞应变片体积描记法，对47名年龄在55±1岁的2型糖尿病中年男性和女性，以及15名年龄匹配的健康个体（52±3岁）进行了前臂基础微循环血流量（FBF）检查，所有受试者均服用阿司匹林。在向肱动脉输注N(G)-单甲基-L-精氨酸以抑制基础一氧化氮释放后（FBF+L-NMMA），也对血流量进行了测量。给予乙酰胆碱（ACh）和硝普钠（SNP）以评估内皮依赖性和非内皮依赖性功能。与对照组相比，糖尿病受试者对ACh和SNP的血管舒张反应显著降低（每项p<0.05）。与对照组相比，糖尿病受试者的基础FBF和FBF+L-NMMA升高（分别为2.4±0.2 ml/100ml/min对1.7±0.2 ml/100ml/min，p=0.02；以及1.9±0.1 ml/100ml/min对1.2+0.1 ml/100ml/min，p=0.01），而L-NMMA后FBF的变化在对照组中更大（-27%对-19%，p=0.05）。在糖尿病受试者中，脉压和高密度脂蛋白胆固醇是FBF（分别为b=0.04±0.01，调整后r2=0.21，p=0.001；以及b=3.3±1.2，调整后r2=0.12，p=0.007）和FBF+L-NMMA（分别为b=0.03±0.01，调整后r2=0.20，p=0.002；以及b=2.1±0.9，调整后r2=0.09，p=0.02）的独立预测因素。舒张压预测了L-NMMA引起的FBF变化（b=-1.02±0.32，调整后r2=0.20，p=0.003）。我们的研究结果表明，血糖控制良好的2型糖尿病患者前臂阻力动脉的激动剂介导的血管舒张受损，这与基础一氧化氮释放受损但非一氧化氮血管舒张剂释放增加有关。后者可能是对动脉僵硬度增加的一种代偿反应，并且可能受高密度脂蛋白的作用促进。
