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目的探讨实验大鼠急性心肌梗死(AMI)后心功能改变和心肌梗死(MI)范围、凋亡、炎症的病理演变规律及相关机制。方法雄性Wistar大鼠68只,随机分MI(结扎冠状动脉左前降支)组(n=40)及相应假手术(Sham,只挂线不结扎冠状动脉)组(n=28)。MI组(3 h内死亡12只)分MI后1、7、14和28 d组,分别于术后观察期满导管法检测血流动力学改变,并取心脏组织行苏木素伊红(HE)、氯化四唑(TTC)、Masson染色观察病理变化,末端脱氧核糖核苷酸转移酶介导的dUTP缺口末端标记法(TUNEL)染色检测凋亡,免疫组化检测炎症细胞密度及转化生长因子β1(TGF-β1)的表达。Western blot检测血管细胞黏附分子-1(VCAM-1)、TGF-β1的表达,实时PCR法检测VCAM-1、单核细胞趋化因子1(MCP-1)的表达。结果MI后1～14 d心功能明显下降,28 d未明显恶化。MI后1、7、14及28 d组梗死范围分别为(41±3)%、(37±3)%、(38±3)%和(28±3)%,凋亡率分别为(46.3±3.0)%、(3.8±2.1)%、(3.3±2.3)%和(1.4±1.0)%,炎症细胞密度分别为(630±72)个/mm2、(1360±102)个/mm2、(1000±98)个/mm2和(223±13)个/mm2,而相应Sham组各种指标均为正常。VCAM-1、MCP-1的表达在MI后1 d明显升高,14 d后下降。TGF-β1在MI后始终处于高表达。结论大鼠MI后其凋亡高峰在1 d,炎症反应高峰在7 d出现,28 d后基本完成MI后修复过程。
Objective To investigate the changes of cardiac function and the range of myocardial infarction (MI), apoptosis and inflammation in experimental rats after acute myocardial infarction (AMI) and the related mechanisms. Methods Sixty-eight male Wistar rats were randomly divided into MI group (n = 40) and sham group (n = 28). The MI group (12 deaths within 3 h) was divided into 1, 7, 14 and 28 d groups after MI, and the hemodynamic changes were examined by expiration after the operation. The HE staining was performed on the heart tissue, (TTC) and Masson staining were used to observe the pathological changes. Apoptosis was detected by terminal deoxynucleotidyl transferase mediated dUTP nick end labeling (TUNEL) staining. Inflammatory cell density and expression of transforming growth factor β1 (TGF-β1) expression. The expressions of VCAM-1 and TGF-β1 were detected by Western blot. The expressions of VCAM-1 and MCP-1 were detected by real-time PCR. Results After 1 to 14 days of MI, heart function decreased significantly and no significant deterioration occurred on the 28th day. The infarct size was (41 ± 3)%, (37 ± 3)%, (38 ± 3)% and (28 ± 3)% respectively at 1, 7, 14 and 28 d after MI. The apoptotic rates were (46.3 The mean number of inflammatory cells were (630 ± 72) / mm2, (1360 ± 102) / mm2, 1000 ± 98) pieces / mm2 and (223 ± 13) pieces / mm2, while the corresponding indexes of Sham group were all normal. The expression of VCAM-1 and MCP-1 were significantly increased on the 1st day after MI, and decreased on the 14th day. TGF-β1 is always highly expressed after MI. Conclusions The peak of apoptosis in MI rats is at 1 day and the peak of inflammatory reaction occurs at 7 days. After 28 days, the process of MI repair is basically completed.