Cai D, Yu B, Yan T
Research Unit of Endocrinology, Sun Yat-Sen University of Medical Science, Guangzhou.
Zhonghua Yi Xue Za Zhi. 1995 Aug;75(8):476-8, 510-1.
Using fura-2, a fluorescence indicator, we evaluated the changes of platelet cytosolic free calcium concentration ([Ca2+]i) and its role in regulation of thromboxane B2 (TXB2) synthesis in patients with diabetes mellitus (DM group, n = 27) and in healthy subjects (control group, n = 15). The A23187-evoked elevation of [Ca2+]i and TXB2 production were higher in the DM group than in the control group (P < 0.01 respectively). The rise in [Ca2+]i was correlated positively with TXB2 production. In contrast, stimulation with arachidonic acid, TXB2 production was unaltered between the groups, although arachidonate-induced [Ca2+]i was higher in the DM group than in the control group (P < 0.05). The results suggested that changes in platelets [Ca2+]i in diabetic subjects may contribute to increase in TXB2 synthesis, involved libration of free arachidonate from membrance phospholipids by the action of phospholipases. Since no significant difference was found between the diabetic patients with microangiopathy (n = 13) and without microangiopathy (n = 14), the results above may be involved in the development of diabetic microangiopathy.
我们使用荧光指示剂fura-2评估了糖尿病患者（糖尿病组，n = 27）和健康受试者（对照组，n = 15）血小板胞质游离钙浓度（[Ca2+]i）的变化及其在血栓素B2（TXB2）合成调节中的作用。糖尿病组中A23187诱导的[Ca2+]i升高和TXB2生成均高于对照组（P均<0.01）。[Ca2+]i的升高与TXB2生成呈正相关。相反，用花生四烯酸刺激时，尽管糖尿病组花生四烯酸诱导的[Ca2+]i高于对照组（P < 0.05），但两组间TXB2生成未发生改变。结果提示，糖尿病患者血小板[Ca2+]i的变化可能有助于TXB2合成增加，这涉及磷脂酶作用使膜磷脂释放游离花生四烯酸。由于在有微血管病变的糖尿病患者（n = 13）和无微血管病变的糖尿病患者（n = 14）之间未发现显著差异，上述结果可能与糖尿病微血管病变的发生有关。
