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目的 :探讨急性心肌梗塞后 ,梗塞区心肌间质金属蛋白酶 (MMPs)活性的动态变化及洛沙坦对其的影响。方法 :结扎SD大鼠冠状动脉前降支复制急性心梗模型 ,随机分成对照组和用药组。采用MPA -V型多导生物信号分析系统监测血流动力学指标 ;采用酶谱法测定 5 4kD间质金属蛋白酶 1(MMP - 1)、5 8kD和 6 2kD间质金属蛋白酶 2 (MMP - 2 )的活性 ;采用氯氨T法测定胶原蛋白的含量。结果 :梗塞区MMPs活性表现出 -过性升高 ,第 3d比假手术组高 4 5倍 ,第 7d高 6 5倍达高峰 ,然后下降 ,第 14d降至 2倍 ,第 42d仍高 1 5倍。用药组MMP - 1比同时间点对照组降低 33% ,MMP - 2低至 5 0 % ;左室重量与体重之比 (LVW/BW ) ,第 14d和第 42d明显低于对照组 (P <0 0 1) ;梗塞区胶原密度第 42d显著低于假手术组 (P <0 0 1)。用药组心脏舒张末期压力于第 3d一过性高于对照组 ,第 7、14、42d均低于对照组。收缩压最大上升速度高于对照组 (P <0 0 5 )。结论 :心肌梗塞后梗塞区MMPs被激活 ,加速胶原分解代谢 ;洛沙坦降低MMPs活性 ,降低胶原分解代谢 ,同时抑制胶原合成代谢 ,使心梗后期胶原含量降低 ,具有改善心脏功能 ,保护心肌的作用
Objective: To investigate the dynamic changes of myocardial interstitial metalloproteinases (MMPs) in infarcted area and the effect of losartan on them after acute myocardial infarction. Methods: Acute myocardial infarction (AMI) model was established by ligating the anterior descending coronary artery of SD rats and randomly divided into control group and treatment group. The MPA - V multi - guided bioassay system was used to monitor the hemodynamic parameters. The enzyme - linked immunosorbent assay (ELISA) was used to detect the expression of MMP - 1 and MMP - 2, 58kD and 62kD MMP - ) Activity; Determination of collagen content by chloramine T method. Results: The MMPs activity in the infarcted area showed a transient increase. The levels of MMPs in the infarcted area were 45 times higher than those in the sham operation group and 65 times higher than those in the sham operation group at the third day, then decreased and decreased to 2 times on the 14th day, Times Compared with the control group, MMP - 1 decreased by 33% and MMP - 2 decreased by 50% compared with the control group at the same time. The ratio of LVW / BW was significantly lower at the 14th and 42th days than that in the control group (P < 0 0 1). Collagen density in the infarcted area was significantly lower on the 42th day than that of the sham operation group (P <0.01). Cardiac end-diastolic pressure in the medication group was higher than that in the control group on the third day, and was lower on the 7th, 14th and 42nd day than that of the control group. The maximum rate of systolic blood pressure increased faster than the control group (P <0 05). Conclusion: MMPs are activated in the infarct area after myocardial infarction, accelerating the catabolism of collagen. Losartan can reduce the activity of MMPs, reduce the catabolism of collagen, inhibit the synthesis and metabolism of collagen, reduce the content of collagen in the late stage of myocardial infarction, improve cardiac function and protect myocardium effect