Evaluation of Endothelial Function Using High-Resolution Ultrasound in Normal Subjects: Endothelial Function according to Aging

BACKGROUND AND OBJECTIVES: Flow-mediated brachial artery vasoactivity has been proposed as a noninvasive means for assessing endothelial function. The present study is designed to assess the influence of aging on endothelial function and when vasoactivity developed initially, peaked. MATERIALS AND METHOD: We measured brachial artery diameter for 60 seconds continuously using 7.5 MHz ultrasound following 5 minutes of lower arm occlusion in 22 normal volun-teers (young group: 10 volunteers, 26.5+/-1.9 years; old group: 12 volunteers, 55.9+/-3.3 years). After sublingual administration of 0.6 mg nitroglycerine, 240 seconds continuously. And then we measure vasoactivity every 3 seconds. RESULTS: Flow-mediated vasodilation (FMD) was started earlier in young group (24.3+/-2.8 sec; old group 28.8+/-3.6 sec, p=0.017). After release of occlusion, peak vasoacitivity time was at 35.5+/-4.7 seconds and peak vasoactivity was 8.4+/-1.7% in young group (old group 6.9+/-1.5%, p=0.099). Endothelial independent vasodilation (EID) was started at 80.7+/-13.3 seconds after sublingual nitroglycerine in young group (vs 80.0+/-19.0 sec), peaked at 177.5+/-16.9 seconds (vs 171.3+/-13.8 sec). Peak vasoactivity was higher in young group (19.1+/-3.1%; old group 15.9+/-2.5%, p=0.033). CONCLUSION: We conclude that 1) Aging has influence on endothelial function about initiating time of vasoactivity as well as peak vaso- activity. 2) FMD can be measured around 50 seconds after release of brachial artery occlusion and EID at 180 seconds after application of sublingual nitroglycerine. 3) The initiating time of vasoactivity (under 30 seconds) can be used for evaluation of endothelial function.

The Effects of Glucose , Insulin and Angiotensin II on Plasminogen Activator Inhibitor-1 Expression and Growth of Aortic Vascular Smooth Muscle Cell in Rats / 대한흉부외과학회지

BACKGROUND: Plasminogen activator inhibitor-1(PAI-1) is known as the primary physiological inhibitor of tissue-type plasminogen activator(t-PA) in the plasma, and is present within the atherosclerotic vessels. Increased plasma levels of PAI-1 are one of the major disturbances of the hemostatic system in patients with diabetes and/or hypertension, and may have multiple interrelations with the important risk factors in the development of atherosclerosis. This study was performed to determine whether altered gene expression of PAI-1 occurs within the arterial wall, and thereby potentially contributing to the increase of cardiovascular risks associated with diabetes and/or hypertension. MATERIAL AND METHOD: The aortic vascular smooth muscle cells of the rat were exposed to 22 mM glucose, angiotensin II, and insulin increased PAI-1 mRNA expression with the use of Northern blotting were examined. Also examined were the effects of 22 mM glucose, angiotensin II and insulin on the growth of the rat's aortic smooth muscle cells by using MTT assay. RESULT: Twenty-two mM glucose treatment increased the PAI-1 mRNA expression in a time- and dose-dependent manner. Aniotensin II treatment synergistically increased the glucose-induced PAI-1 mRNA expression. In contrast, addition of insulin attenuated the increase of 22 mM glucose and angiotensin II induced PAI-1 mRNA expression. Furthermore, treatment of 22 mM glucose, angiotensin II and insulin resulted in a significant increase in cell numbers. This study demonstrated that 22 mM glucose and angiotensin II have a synergistic effect in stimulating the PAI-1 mRNA expression and in the cell growth of the rat's aortic smooth muscle cells. CONCLUSION: Elevation of glucose and angiotensin II may be important risk factors in impairing fibrinolysis and developing atherosclerosis in diabetic patients.