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目的 :探讨血糖对黏附分子的影响及其在LI发病机制中的作用。方法 :采用流式细胞术对LI合并Ⅱ型糖尿病及非糖尿病LI病人外周血白细胞的膜糖蛋白CD11b、CD18和血小板膜糖蛋白CD62p的表达进行检测。结果 :两组病人比较血小板膜糖蛋白CD62p、白细胞膜糖蛋白CD11b、CD18表达在腔隙性脑梗死合并糖尿病组明显高于非糖尿病腔隙性脑梗死组 ;血糖与CD62p、CD11b呈正相关 ;CD62p、CD11b、CD18及血糖与LI腔梗个数无关。结论 :超负荷血糖时血小板、白细胞均处于高活化状态。超负荷血糖导致的细胞黏附分子的高表达参与LI微血管病变的损伤过程。
Objective: To investigate the effect of blood glucose on adhesion molecules and its role in the pathogenesis of LI. Methods: The expression of membrane glycoprotein CD11b, CD18 and platelet membrane glycoprotein CD62p in peripheral leukocytes of LI patients with type II diabetes mellitus and with non-diabetic patients LI were detected by flow cytometry. Results: The expression of platelet membrane glycoprotein CD62p, leukocyte glycoprotein CD11b and CD18 were significantly higher in patients with lacunar infarction with diabetes mellitus than those without lacunar infarction. The levels of CD62p and CD11b were positively correlated with the level of CD62p , CD11b, CD18 and blood sugar and the number of LI cavity stem has nothing to do. Conclusion: Platelets and leucocytes are highly activated when blood glucose is overloaded. Hyperglycemia leads to the high expression of cell adhesion molecules involved in the lesion process of LI microvascular lesions.