急性冠脉综合征患者循环血单核细胞产生明胶酶增加

目的 :探讨单核细胞产生两种明胶酶 (MMP2 ,MMP9)与急性冠脉综合征 (ACS)发病间的关系。方法 :分离 38例不稳定心绞痛 (UA)、16例心肌梗死 (AMI) ,2 2例稳定性心绞痛 (SA)及 18例正常对照 (CONT)循环血单核细胞 ,在体外无血清培养 2 4h ,测定上清液中MMP2、MMP9蛋白含量 ,并观察心肌缺血及心肌梗死对其的影响。结果 :UA、AMI组MMP2分别高于CONT组 (2 6 5 8 5 2± 5 33 42和 1842 34± 317 17,P <0 0 0 1,单位为 μg/L ,下同 ;2 6 43 0 4± 6 41 47和 1842 34± 317 17,P <0 0 0 1)和SA组 (2 6 5 8 5 2± 5 33 42和 1919 16± 2 89 38,P <0 0 0 1;2 6 43 0 4± 6 41 47和 1919 16± 2 89 38,P <0 0 0 1)。UA、AMI组MMP9也分别高于CONT组 (481 41± 5 2 5 6和 30 1 2 6± 30 17,P <0 0 0 1;486 34± 37 48和 30 1 2 6± 30 17,P <0 0 0 1)和SA组 (481 41± 5 2 5 6和 2 98 86± 42 2 4,P <0 0 0 1;486 34± 37 48和 2 98 86± 42 2 4,P <0 0 0 1)。心肌缺血发作前后MMP2、MMP9无显著变化 ,心肌梗死 72h内仍保持在发病初期水平 ,梗死后多个时间点及其最大值与CK或Ck MB相应时间点及其最大值间无线性相关。结论 :急性冠脉综合征患者循环血单核细胞产生MMP2、MMP9增加 ,MMP2、MMP9不受心肌

The productions of gelatinases from circulating monocytes were increased in patients with acute coronary syndrome

Objective:To investigate the productions of MMP2 and MMP9 from circulating monocytes in patients with acute coronary syndrome, and alternations of them after myocardial ischemia or myocardial infarction, and to discuss the action of these two gelatinases on pathogenesis of acute coronary syndrome Methods:The contents of MMP2 and MMP9 in supermatart of cultural monocytes from 38 UA, 16AMI, 22 SApatients and 18 Control subjects were measured by ELISA kit Moreover, the alternations of two gelatinases after myocardiaol ischemia, in the time course of myocardial infarction, and the relationship between MMP2, MMP9 and serum Ck/Ck MB were analyzed respectively Results:The productions of MMP2 and MMP9 of circualting mnocytes from patients with UA, AMI group were greater than those from control subjects ( MMP2: P < 0 001; MMP9: P < 0 001) and patients with SA(MMP2: P < 0 001; MMP9: P < 0 001) The contents of MMP2 and MMP9 were almost unchanged after onset of myocardiaol ischemia or in the first 72 hours after myocardial infarction, and they were not correlated with serum Ck/Ck MB Conclusion:The productions of MMP2 and MMP9 in circulating monocytes from patients with UA and AMI were increased, and were not affected by myocardiol ischemia or infarction As a result, they might participate in pathogenesis of acute coronary syndrome.