欢迎访问《解剖学报》官方网站！今天是
English
大鼠心肌梗死后心功能变化与新生血管的关系
Relationship between cardiac function and angiogenesis after rat myocardial infarction
目的 探讨大鼠心肌梗死后心功能变化及其与血管新生之间的关系。 方法 结扎大鼠左冠状动脉前降支，制备心肌梗死模型，术后利用心脏彩超分别评价梗死后1周、2周、3周和4周的心功能，采用免疫组织化学和Western blotting方法，检测各周大鼠梗死边缘Ⅷ因子和血管内皮生长因子（VEGF）的表达变化。结果 大鼠心肌梗死1周时心功能最差，2周和3周心功能有所改善，4周时心功能降低；Ⅷ因子与VEGF于术后1周、2周呈高表达，3周表达开始降低，4周时已接近正常水平。 结论 梗死后心功能的变化与血管新生不一致，心肌梗死早期血管密度的增加不能明显改善心功能。
Objective To explore the relationship between changes of heart function and angiogenesis after myocardial infarction, and provide morphological reference for clinical treatment of myocardial infarction. Methods Acute myocardiac infarction (AMI) model was established with Sprague-Dawley rats by ligation of the left anterior descending coronary artery.Cardiac function at different weeks after AMI was evaluated by echocardiography. The change of Ⅷ factor and vascular endothelial growth factor（VEGF）expression at the infarction edge in rats hearts at each week after AMI was detected by immunohistochemistry and Western blotting. Results The cardiac function of 1W after myocardial infarction was worst, cardiac function was improved during 2 weeks and 3weeks, but reduced at the 4th week; Ⅷ factor and VEGF in post-myocardial infarction 1 week, 2 weeks were highly expressed. Expression of both factors began to decrease at the 3rd week. At the 4th week, expression levels were close to normal. Conclusion The change of cardiac function after myocardial infarction is inconsistent with that of angiogenesis, early increased vascular density can not obviously improve cardiac function.
Ⅷ因子 / 血管内皮生长因子 / 心肌梗死 / 新生血管 / 心脏彩超 / 免疫组织化学 / 免疫印迹法 / 大鼠
Factor Ⅷ / Vascular endothelial growth factor / Myocardial infarction / Angiogenesis / Echocardiography / Immunohistochemistry / Western blotting / Rat
［1］Silvestre JS, Smadja DM, Lévy BI. Postischemic revascularization: from cellular and molecular mechanisms to clinical applications［J］. Physiol Rev, 2013, 93(4):1743-1802.
［2］Falls DL. Neuregulins:functions,forms,and signaling strategies［J］. Exp Cell Res, 2003, 284（2）:14-30.
［3］Tang YL，Zhao Q，Qin X，et al.Paraerine action enhances the effects of autologous mesenchymal stem cell transplantation on vascular regeneration in rat model of myocardial infarction ［J］. Ann Thorac Surs, 2005, 80(1): 229-236.
［4］Lopez AD, Mathers CD, Ezzati M, et al. Global and regional burden of disease and risk factors, 2001: systematic analysis of population health data ［J］. Lancet, 2006, 367（3）:1747-1757.
［5］Virag JA, Rolle ML, Reece J, et al. Fibroblast growth factor-2 regulates myocardial infarct repair: effects on cell proliferation, scar contraction, and ventricular function ［J］. Am J Pathol, 2007, 171（3）:1431-1440.
［6］Miao DM, Cao RH, Liu Y, et al. Dynamics of high-frequency echocardiography for myocardial infarction left ventricular remodeling ［J］. Chinese Journal of Rehabilitation Theory and Practice, 2009, 15 (4) : 308-309. (in Chinese)
苗冬梅，曹瑞华，刘源，等. 高频超声心动图对心肌梗死大鼠左心室重构的动态研究［J］. 中国康复理论与实践，2009，15（4）：308-309.
［7］Jivraj N, Phinikaridou A, Shah AM, et al.Molecular imaging of myocardial infarction［J］. Basic Res Cardiol, 2014, 109(1):397.
［8］Holmes K, Roberts OL, Thomas AM, et al. Vascular endothelial growth factorreceptor-2：structure，function，intracellular signalling and therapeutic inhibition ［J］. Cell Signal, 2007, 19(10): 2003-2012.
［9］O’Shea S，Johnson K，Clark R，et al.Effects of in vivo heregulin beta1 treatment in wild-type and ErbB gene-targeted mice depend on receptor levels and pregnancy ［J］. Am J Pathol, 2001, 158(5): 1871-1880.
/
| 〈 |
|
〉 |
