ENDOTHELIUM-DEPENDENT VASODILATATION IS IMPAIRED IN BOTH MICROCIRCULATION AND MACROCIRCULATION DURING ACUTE HYPERGLYCEMIA

Purpose: Endothelial dysfunction is associated with atheromatosis and is a common finding with diabetes. We have studied the effects of acut e hyperglycemia on the endothelium-dependent vasodilatation of both th e microcirculation and the macrocirculation of healthy subjects. Becau se of the presence of endothelial dysfunction with diabetes, we hypoth esize that acute hyperglycemia causes impaired endothelial-dependent r esponses. Methods: Twenty healthy subjects (15 men, 5 women) with a me an age of 32.3 years (range, 23 to 49 years) were examined during fast ing conditions and at 1 hour after the ingestion of 75 g of glucose. T he endothelium-dependent vasodilatation of the brachial artery, a cond uit vessel, was evaluated with high-resolution ultrasound scan to meas ure the changes in the vessel diameter induced with reactive hyperemia . In the microcirculation, the endothelial function was assessed by me asuring the changes in the erythrocyte flux after the acetylcholine io ntophoresis. Results: The brachial artery endothelium-dependent dilata tion was greater during fasting as compared with the response after th e 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 avera ge blood flow velocities during the hyperemic response were higher aft er 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 administra tion of the glucose load (1293% [591 to 1856] vs 863% [385 to 1180]; P < .01). Conclusions: Ln healthy subjects, the ingestion of a glucose load impairs the endothelial-dependent vasodilation in both the microc irculation 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. Fur ther studies are necessary to examine the long-term effects of hypergl ycemia.