Tarutani Yasuhiro, Matsumoto Tetsuya, Takashima Hiroyuki, Yamane Tetsunobu, Horie Minoru
Department of Cardiovascular and Respiratory Medicine, Shiga University of Medical Science, Otsu, Japan.
Hypertens Res. 2005 Jan;28(1):59-66. doi: 10.1291/hypres.28.59.
Endothelium plays a key role in the regulation of not only vascular tone but also thrombosis and fibrinolysis. Brachial flow-mediated vasodilation (FMD) provides a noninvasive method of assessing coronary endothelial dysfunction. However, no data are available on the relationship between brachial FMD and coronary fibrinolytic activity. Thus, we examined the relationship between brachial FMD and coronary vasomotor and fibrinolytic function. Brachial FMD by reactive hyperemia was defined as a change in diameter relative to the baseline as measured using high-resolution ultrasound. Coronary blood flow (CBF) responses to bradykinin (BK) were analyzed using Doppler flow velocity measurement. Coronary release of tissue-type plasminogen activator (tPA) antigen was determined as the transcardiac tPA gradient x [CBF x (100 - hematocrity 100)]. In 77 patients with normal coronary arteries, BK caused dose-dependent increases in CBF, transcardiac tPA gradient, and coronary tPA release. Among them, brachial FMD, the BK-induced CBF increase, and the coronary tPA release induced by BK in 14 diabetic subjects were lower than those in 63 non-diabetic subjects (p < 0.05, respectively). Brachial FMD correlated with the CBF increase, transcardiac tPA gradient (0.2 microg/min: r = 0.25; 0.6 microg/min: r = 0.43; 2.0 microg/min: r = 0.34; p < 0.05, respectively), and coronary tPA release (0.2 microg/min: r = 0.24; 0.6 microg/min: r = 0.44; 2.0 microg/min: r = 0.32; p < 0.05, respectively) in response to BK. Brachial FMD correlated significantly with coronary endothelial function and fibrinolytic activity in response to BK. Type 2 diabetes impaired coronary and brachial endothelium-dependent vasodilation and coronary fibrinolytic activity.
内皮不仅在血管张力调节中起关键作用，而且在血栓形成和纤维蛋白溶解过程中也发挥着重要作用。肱动脉血流介导的血管舒张功能（FMD）为评估冠状动脉内皮功能障碍提供了一种非侵入性方法。然而，目前尚无关于肱动脉FMD与冠状动脉纤维蛋白溶解活性之间关系的数据。因此，我们研究了肱动脉FMD与冠状动脉血管舒缩功能及纤维蛋白溶解功能之间的关系。通过反应性充血测定的肱动脉FMD定义为使用高分辨率超声测量的相对于基线的直径变化。使用多普勒流速测量分析冠状动脉血流（CBF）对缓激肽（BK）的反应。组织型纤溶酶原激活剂（tPA）抗原的冠状动脉释放量通过心腔tPA梯度x [CBF x（100 - 血细胞比容/100）]来确定。在77例冠状动脉正常的患者中，BK引起CBF、心腔tPA梯度和冠状动脉tPA释放量呈剂量依赖性增加。其中，14例糖尿病患者的肱动脉FMD、BK诱导的CBF增加以及BK诱导的冠状动脉tPA释放均低于63例非糖尿病患者（p均<0.05）。肱动脉FMD与BK刺激后的CBF增加、心腔tPA梯度（0.2微克/分钟：r = 0.25；0.6微克/分钟：r = 0.43；2.0微克/分钟：r = 0.34；p均<0.05）以及冠状动脉tPA释放（0.2微克/分钟：r = 0.24；0.6微克/分钟：r = 0.44；2.0微克/分钟：r = 0.32；p均<0.05）相关。肱动脉FMD与BK刺激后的冠状动脉内皮功能和纤维蛋白溶解活性显著相关。2型糖尿病损害了冠状动脉和肱动脉的内皮依赖性血管舒张功能以及冠状动脉纤维蛋白溶解活性。
