Thalhammer C, Balzuweit B, Busjahn A, Walter C, Luft F C, Haller H
Franz Volhard Clinic at the Max Delbrück Center for Molecular Medicine, Universitätsklinikum Charité, Medical Faculty of Humboldt University, Capus Berlin-Buch, Berlin, Germany.
Arterioscler Thromb Vasc Biol. 1999 May;19(5):1173-9. doi: 10.1161/01.atv.19.5.1173.
To investigate the effects of fasting and postprandial glucose on endothelial cell function and intima-media thickness, we studied 60 men with cardiovascular risk factors. Postischemic, endothelium-dependent vasodilatation was measured after 3 minutes of ischemia at the radial artery with high-resolution echo tracking. Common carotid artery intima-media thickness was measured by B-mode ultrasound. Glucose tolerance was determined by a 75-g oral glucose load. Fasting glucose levels were inversely correlated with postischemic, endothelium-dependent vasodilatation (r=-0.24, P<0.05) and directly correlated with intima-media thickness (r=0.26, P<0.05). However, postischemic, endothelium-dependent vasodilatation and intima-media thickness were not correlated. All subjects with normal postischemic, endothelium-dependent vasodilatation also had a normal intima-media thickness, whereas some subjects with impaired postischemic, endothelium-dependent vasodilatation also had a normal intima-media thickness. Multiple regression analysis revealed a profound influence of age on intima-media thickness to the exclusion of all other variables. The same age-adjusted analysis for postischemic, endothelium-dependent vasodilatation accepted fasting glucose, followed by 2-hour postprandial glucose, as variables, but no others. Subjects with fasting glucose values >100 mg/dL showed reduced postischemic, endothelium-dependent vasodilatation (59 versus 120 microm, P<0.05) and a higher intima-media thickness (right: 0.76 versus 0.62 mm, P<0.05; left: 0.78 versus 0.63 mm, P<0. 05) compared with those with fasting glucose values <100 mg/dL. Subjects with 2-hour postprandial glucose values >125 mg/dL had no reduced postischemic, endothelium-dependent vasodilatation compared with subjects with a 2-hour postprandial glucose <125 mg/dL; however, their intima-media thickness (right: 0.66 versus 0.62 mm; left: 0. 68 versus 0.62 mm; P<0.05 for both) was greater. Thus, high fasting rather than postprandial glucose values are associated with both postischemic, endothelium-dependent vasodilatation and increased intima-media thickness. Postischemic endothelium-dependent vasodilatation may precede increased intima-media thickness.
为研究空腹血糖和餐后血糖对内皮细胞功能及内膜中层厚度的影响,我们对60名有心血管危险因素的男性进行了研究。采用高分辨率回声跟踪技术,在桡动脉缺血3分钟后测量缺血后内皮依赖性血管舒张功能。用B型超声测量颈总动脉内膜中层厚度。通过75克口服葡萄糖耐量试验测定葡萄糖耐量。空腹血糖水平与缺血后内皮依赖性血管舒张呈负相关(r = -0.24,P < 0.05),与内膜中层厚度呈正相关(r = 0.26,P < 0.05)。然而,缺血后内皮依赖性血管舒张与内膜中层厚度不相关。所有缺血后内皮依赖性血管舒张功能正常的受试者内膜中层厚度也正常,而一些缺血后内皮依赖性血管舒张功能受损的受试者内膜中层厚度也正常。多元回归分析显示,年龄对内膜中层厚度有显著影响,排除了所有其他变量。对缺血后内皮依赖性血管舒张进行相同的年龄校正分析时,将空腹血糖作为变量,其次是餐后2小时血糖,但没有其他变量。空腹血糖值>100 mg/dL的受试者与空腹血糖值<100 mg/dL的受试者相比,缺血后内皮依赖性血管舒张功能降低(59对120微米,P < 0.05),内膜中层厚度更高(右侧:0.76对0.62毫米,P < 0.05;左侧:0.78对0.63毫米,P < 0.05)。餐后2小时血糖值>125 mg/dL的受试者与餐后2小时血糖<125 mg/dL的受试者相比,缺血后内皮依赖性血管舒张功能没有降低;然而,他们的内膜中层厚度更大(右侧:0.66对0.62毫米;左侧:0.68对0.62毫米;两者P均< 0.05)。因此,空腹血糖高而非餐后血糖高与缺血后内皮依赖性血管舒张及内膜中层厚度增加有关。缺血后内皮依赖性血管舒张可能先于内膜中层厚度增加。