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目的:观察阿司匹林对心梗后诱导的心肌纤维化的预防作用。方法:对大鼠采用左冠动脉结扎建立心梗模型,以随机原则将实验大鼠分为阿司匹林组、模型组和假手术组,建模4周、8周后分别检测3组血流动力学相关参数,之后分离大鼠心脏并观察心肌纤维化相关参数。结果:在血流动力学方面,4周时模型组左心室收缩压(LVSP),左室舒张末期压(LVEDP),左心室最大收缩速率(+d max/dt)及左心室最大舒张速率(-d min/dt)均明显低于假手术组,差异有统计学意义(P均<0.01)。阿司匹林组LVEDP相比模型组明显升高(P<0.05)。8周时模型组LVSP、LVEDP、LVMP、+d max/dt以及-d max/dt均显著低于假手术组(P均<0.05)。阿司匹林组LVSP、LVEDP、LVMP、+d max/dt和-d max/dt相比模型组明显升高(P均<0.05)。心肌纤维化方面:与假手术组相比,4周和8周时模型组LVAW,HL,HL/L维生素D和LVAW/LVD均降低,LVD增大(P均<0.05)。使用了阿司匹林后这些指标均有明显的改善。结论:阿司匹林对心梗后诱导的心肌纤维化有一定的改善作用,这一结论可以为临床预防心梗后诱导的心肌纤维化提供依据。
Objective: To observe the preventive effect of aspirin on myocardial fibrosis induced by myocardial infarction. Methods: The myocardial infarction model was established by ligation of the left coronary artery in rats. The rats were randomly divided into aspirin group, model group and sham operation group. After 4 weeks and 8 weeks, the hemodynamics Related parameters, then isolated rat heart and observed myocardial fibrosis related parameters. Results: In hemodynamics, left ventricular systolic pressure (LVSP), left ventricular end-diastolic pressure (LVEDP), maximal left ventricular systolic velocity (dmax / dt) and maximal left ventricular diastolic velocity -d min / dt) were significantly lower than the sham operation group, the difference was statistically significant (P all <0.01). LVEDP in aspirin group was significantly higher than that in model group (P <0.05). LVSP, LVEDP, LVMP, + d max / dt and -d max / dt of model group were significantly lower than those of sham operation group at 8 weeks (all P <0.05). LVSP, LVEDP, LVMP, + d max / dt and -d max / dt in aspirin group were significantly higher than those in model group (all P <0.05). Compared with the sham operation group, LVAW, HL, HL / L vitamin D and LVAW / LVD decreased and LVD increased at 4 and 8 weeks in model group (all P <0.05). After the use of aspirin these indicators have significantly improved. CONCLUSIONS: Aspirin can improve myocardial fibrosis induced by myocardial infarction. This conclusion may provide a basis for clinical prevention of myocardial fibrosis induced by myocardial infarction.