目的　研究阿司匹林（乙酰水杨酸，ＡＳＡ）对急性心肌梗死（ＡＭＩ）患者血小板与白细胞粘附的影响及其作用机制。方法　采用体外玫瑰花结形成实验检测血小板与白细胞粘附，观察ＡＳＡ 对两者粘附的作用；用１２５Ｉ标记的单克隆抗体测定血小板表面α颗粒膜蛋白１４０（ＧＭＰ１４０）的表达，观察ＡＳＡ对凝血酶诱导的血小板表面ＧＭＰ１４０ 表达的影响。结果　ＡＭＩ患者血小板与白细胞间粘附率增高，凝血酶通过诱导血小板表面ＧＭＰ１４０ 的表达促进血小板与白细胞粘附；阿司匹林（５００、５ ０００μｇ／ｍ ｌ）抑制ＡＭＩ患者血小板与白细胞间的粘附，抑制凝血酶诱导的正常人血小板与白细胞间的粘附以及凝血酶诱导的血小板表面ＧＭＰ１４０ 的表达。结论　ＡＳＡ一方面通过抑制ＧＭＰ１４０ 的表达，另一方面可能通过影响配体间的结合抑制血小板与白细胞之间的粘附，揭示了ＡＳＡ 抗栓作用的另外一种机制 Objective To study the effect of aspirin (ASA) on platelet and leukocyte adhesion in patients with acute myocardial infarction (AMI) and its mechanism. Methods In vitro rosette formation assay was used to detect the adhesion of platelets and leukocytes to observe the effect of ASA on their adhesion. The expression of α-granule membrane protein-140 (GMP140) on platelet surface was measured by 125I labeled monoclonal antibody. ASA on thrombin-induced platelet surface GMP 140 expression. Results The adhesion rate of platelets and leukocytes in AMI patients was increased. Thrombin promoted the adhesion of platelets and leucocytes by inducing the expression of GMP-140 on platelet surface. Aspirin (500 and 5 000 μg / ml) inhibited the adhesion between platelets and leukocytes in AMI patients , Inhibition of thrombin-induced normal human platelet and white blood cell adhesion and thrombin-induced platelet surface GMP 140 expression. Conclusion ASA on the one hand by inhibiting the expression of GMP 140, on the other hand may affect the binding of ligands to inhibit adhesion between platelets and leukocytes, revealing ASA antithrombotic another mechanism