Akbari C M, Saouaf R, Barnhill D F, Newman P A, LoGerfo F W, Veves A
Department of Surgery, Beth Israel-Deaconess Medical Center, Harvard Medical School, Boston, Mass 02215, USA.
J Vasc Surg. 1998 Oct;28(4):687-94. doi: 10.1016/s0741-5214(98)70095-3.
Endothelial dysfunction is associated with atheromatosis and is a common finding with diabetes. We have studied the effects of acute hyperglycemia on the endothelium-dependent vasodilatation of both the microcirculation and the macrocirculation of healthy subjects. Because of the presence of endothelial dysfunction with diabetes, we hypothesize that acute hyperglycemia causes impaired endothelial-dependent responses.
Twenty healthy subjects (15 men, 5 women) with a mean age of 32.3 years (range, 23 to 49 years) were examined during fasting conditions and at 1 hour after the ingestion of 75 g of glucose. The endothelium-dependent vasodilatation of the brachial artery, a conduit vessel, was evaluated with high-resolution ultrasound scan to measure the changes in the vessel diameter induced with reactive hyperemia. In the microcirculation, the endothelial function was assessed by measuring the changes in the erythrocyte flux after the acetylcholine iontophoresis.
The brachial artery endothelium-dependent dilatation was greater during fasting as compared with the response after the glucose load was administered (11.7% [8.3 to 14.3] vs 4.2% [1.5 to 9.6]; P < .001; median, first, and third quartile). Both peak and average blood flow velocities during the hyperemic response were higher after the administration of the glucose load as compared with the fasting period (P < .05), but no changes were found in the blood flow volume. During fasting, microcirculatory endothelial-dependent vasodilatation was also significantly greater than the response after the administration of the glucose load (1293% [591 to 1856] vs 863% [385 to 1180]; P < .01).
In healthy subjects, the ingestion of a glucose load impairs the endothelial-dependent vasodilation in both the microcirculation and the macrocirculation. Because impairment of endothelial responses is associated with the early changes of atherosclerosis, it is possible that prolonged hyperglycemia and endothelial dysfunction may lead to the early and accelerated atherosclerosis of diabetes. Further studies are necessary to examine the long-term effects of hyperglycemia.
内皮功能障碍与动脉粥样硬化相关，且在糖尿病患者中很常见。我们研究了急性高血糖对健康受试者微循环和大循环中内皮依赖性血管舒张的影响。鉴于糖尿病患者存在内皮功能障碍，我们推测急性高血糖会导致内皮依赖性反应受损。
对20名健康受试者（15名男性，5名女性）进行检查，他们的平均年龄为32.3岁（范围为23至49岁），检查在空腹状态下以及摄入75克葡萄糖后1小时进行。使用高分辨率超声扫描评估肱动脉（一种传导血管）的内皮依赖性血管舒张，以测量反应性充血引起的血管直径变化。在微循环中，通过测量乙酰胆碱离子电渗后红细胞通量的变化来评估内皮功能。
与给予葡萄糖负荷后的反应相比，空腹时肱动脉内皮依赖性扩张更大（11.7% [8.3至14.3] 对4.2% [1.5至9.6]；P <.001；中位数、第一和第三四分位数）。与空腹期相比，给予葡萄糖负荷后充血反应期间的峰值和平均血流速度更高（P <.05），但血流量没有变化。在空腹时，微循环内皮依赖性血管舒张也明显大于给予葡萄糖负荷后的反应（1293% [591至1856] 对863% [385至1180]；P <.01）。
在健康受试者中，摄入葡萄糖负荷会损害微循环和大循环中的内皮依赖性血管舒张。由于内皮反应受损与动脉粥样硬化的早期变化相关，长期高血糖和内皮功能障碍可能导致糖尿病患者早期和加速的动脉粥样硬化。有必要进一步研究以检查高血糖的长期影响。
