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目的对急性心肌梗死(myocardial infarction,MI)大鼠进行双侧肾交感神经切除,探讨去肾交感神经术(renal sympathetic denervation,RDN)能否缓解MI后心室重构并进行可能的机制探讨。方法结扎大鼠左冠状动脉前降支构建MI模型,实验分组为:MI组(n=10)、MI+RDN组(MI建模1周后进行RDN,n=10)和假手术组(n=10)。MI建模4周后对各组大鼠进行超声心动图检查测定心室重构程度和左心功能,对梗死边缘区心肌进行Masson染色观察心肌纤维化程度,免疫组化检测Ⅰ型胶原、Ⅲ型胶原和转化生长因子β1(transforming growth factorβ1,TGF-β1)的表达。结果与MI组相比,MI+RDN组的左室射血分数(ejection fraction,EF)和短轴缩短率(fractional shortening,FS)升高,左室收缩末期内径(left ventricular internal dimensions at end systole,LVIDS)和左室舒张末期内径(left ventricular internal dimensions at end diastole,LVIDD)减少(P均<0.05)。心肌Masson染色结果显示,MI+RDN组大鼠梗死边缘区的心肌纤维化程度较MI组减轻。免疫组化检测显示,与MI组相比,MI+RDN组大鼠梗死边缘区的Ⅰ型胶原、Ⅲ型胶原和TGF-β1表达减少(P均<0.05)。结论RDN可以改善MI大鼠心室重构,提高左心收缩功能,其机制可能与局部下调心肌TGF-β1表达进而减少Ⅰ型胶原和Ⅲ型胶原沉积有关。
Objective To investigate the effect of renal sympathetic denervation (RDN) on the remodeling of ventricular remodeling after MI in rats with acute myocardial infarction (MI). Methods The MI model was established by ligation of the left anterior descending coronary artery of rats. The experimental groups were MI (n = 10), MI + RDN (RDN, n = 10) = 10). Four weeks after MI modeling, the degree of ventricular remodeling and left ventricular function were determined by echocardiography. Masson staining was performed on the marginal zone of myocardial infarction to observe the degree of myocardial fibrosis. Immunohistochemistry was used to detect type Ⅰ collagen, type Ⅲ Collagen and transforming growth factor β1 (TGF-β1) expression. Results Compared with MI group, ejection fraction (EF) and fractional shortening (FS) were increased in MI + RDN group, and left ventricular internal dimensions at end systole , LVIDS) and left ventricular internal dimensions at end diastole (LVIDD) decreased (all P <0.05). Myocardial Masson staining showed that myocardial fibrosis in MI + RDN group was less than that in MI group. Immunohistochemistry showed that the expression of type I collagen, type III collagen and TGF-β1 in MI + RDN group decreased compared with MI group (all P <0.05). Conclusions RDN can improve ventricular remodeling and increase left ventricular systolic function in MI rats. The mechanism may be related to the down-regulation of TGF-β1 expression in myocardium and the reduction of type Ⅰ collagen and type Ⅲ collagen deposition.