大鼠心肌梗死区胶原纤维和弹力纤维的动态变化及其与心功能的关系

发布时间：2018-08-25 12:56

【摘要】：背景急性心肌梗死(Acute myocardiac infarction,AMI)是一种严重危害人类健康的高风险临床常见病。AMI后梗死区域逐渐被瘢痕组织所替代,严重影响心功能,甚至出现心力衰竭。在整个心肌梗死区域变化过程中,不仅心肌细胞发生变化,细胞间质中的各种成分尤其是间质中的胶原纤维和弹力纤维均发生了重大改变。目前对心肌梗死后心肌细胞的变化和毛细血管的新生研究较多,有关心肌间质中弹性纤维和胶原纤维的动态变化及其与心功能变化的关系研究较少。目的探讨大鼠急性心肌梗死后,梗死区域瘢痕组织细胞间质中I型胶原纤维、III型胶原纤维和弹力纤维不同周次的动态变化以及和心功能的关系,旨在为临床心肌梗死后再生提供新的研究思路,为心肌梗死后的临床治疗提供实验证据和理论参考。方法(1)随机将50只SD大鼠分为两组,其中对照组10只,实验组40只。对照组开胸暴露心脏后,为了降低影响只穿线不结扎冠状动脉左前降支,实验组则通过将冠状动脉前降支结扎来制备大鼠心肌梗死模型,术中通过小动物心电图初步检测梗死模型制备情况;(2)小动物B超仪监测每周两组大鼠心功能的动态变化,组织切片,Masson染色检测模型的病理变化;(3)免疫组织化学、免疫荧光和Western Blotting技术检测I型胶原纤维、III型胶原纤维和弹力纤维在对照组和梗死后1周、2周、3周和4周心肌梗死区域的动态变化。结果(1)术中可以看到,结扎左冠状动脉前降支后,结扎点以下部位的心肌呈现青紫色或灰白色,左心耳充血明显,心脏搏动减弱;与对照组对比,梗死组结扎后20分钟心电图II导联ST段显著移位,呈现出ST段弓背型向上抬高约0.2m V,说明术中结扎成功,心梗模型初步建立;(2)对照组和实验组梗死后1周、2周、3周和4周的心功能对比显示,实验组模型大鼠心功能呈现下降趋势:对照组大鼠心功能为(74.90%±4.13),实验组梗死后第1周(58.00%±2.38),梗死第2周(51.74%±2.16),第3周(37.50%±3.00),第4周降至(28.92%±2.83)。且随着梗死周次的增加,LVFS、IVS均逐渐降低,LVIDd、LVIDs逐渐增大,但LVWP变化没有规律。表明心功能受损,且随着梗死周次的增加,心功能逐渐降低,2-3周降低最明显,提示心肌梗死模型制备成功;(3)梗死组各周次组织切片显示,正常心肌呈现红色,胶原纤维被染成绿色,左心室的前壁梗死区明显变薄,纤维组织代替正常心肌进而形成瘢痕,证明心肌梗死模型制备成功;(4)在心肌梗死区域,随梗死时间延长,弹力纤维呈递减趋势:对照组心肌弹力纤维含量为(0.97±0.05),梗死后1周为(0.95±0.04),第2周为(0.22±0.01),第3周为(0.13±0.01),梗死后4周组为(0.03±0.004);(5)I型胶原纤维含量逐渐增加,对照组为(0.471±0.035),梗死后第1周(0.632±0.045),2周组为(0.925±0.107),第3周为(1.071±0.099),4周组为(1.114±0.057);(6)随梗死时间延长,III型胶原含量逐渐增加,对照组为(0.335±0.078),梗死后第1周(0.374±0.018),2周组为(0.469±0.035),梗死3周(0.578±0.021),第4周组为(1.134±0.039)。结论(1)心肌梗死后,时间越长,梗死区域I型和III型胶原纤维含量逐渐增多,而弹力纤维成分逐渐下降,这些蛋白的重构可能是梗死后瘢痕区域僵硬度增加、弹性下降的病理学基础。(2)心功能的降低与弹性纤维减少正相关,与胶原的增加反相关。
[Abstract]:BACKGROUND Acute myocardial infarction (AMI) is a high-risk clinical common disease that seriously endangers human health. After AMI, the infarct area is gradually replaced by scar tissue, seriously affecting cardiac function, and even heart failure. There are many studies on the changes of myocardial cells and capillary angiogenesis after myocardial infarction. There are few studies on the dynamic changes of elastic fibers and collagen fibers in myocardial interstitium and their relationship with cardiac function. Dynamic changes of type I collagen fibers, type III collagen fibers and elastic fibers in the interstitium of scar tissue and their relationship with cardiac function after acute myocardial infarction in rats were studied in order to provide new research ideas for regeneration after myocardial infarction and provide experimental evidence and theoretical reference for clinical treatment after myocardial infarction. Methods (1) Fifty SD rats were randomly divided into two groups: control group (10 rats) and experimental group (40 rats). In the control group, the left anterior descending coronary artery (LAD) was ligated by ligating the anterior descending coronary artery (ADC) in order to reduce the influence of ligating the left anterior descending coronary artery (LAD) after thoracotomy. (3) Collagen type I fibers, collagen type III fibers and elastic fibers were detected by immunohistochemistry, immunofluorescence and Western Blotting techniques in the control group and 1, 2 and 3 weeks after infarction. Results (1) After ligation of the anterior descending branch of the left coronary artery, the myocardium below the ligation point was cyan-purple or grey-white, the left atrial appendage was congested and the heart beat was weakened. Compared with the control group, the ST segment of lead II in the infarction group shifted significantly 20 minutes after ligation, showing a ST segment arch. Back shape was elevated about 0.2 mV, indicating that the intraoperative ligation was successful and the myocardial infarction model was initially established; (2) The comparison of cardiac function between the control group and the experimental group showed that the cardiac function of the experimental group showed a downward trend: the cardiac function of the control group was (74.90% + 4.13), the experimental group was (58.00% + 2.38) in the first week after infarction, and the experimental group was (2.38) in the second week after infarction. LVFS and IVS decreased gradually with the increase of infarction cycle, LVIDd and LVIDs increased gradually, but LVWP did not change regularly. It showed that cardiac function was impaired, and with the increase of infarction cycle, cardiac function gradually decreased, and the most obvious decrease was in 2-3 weeks, suggesting that the model of myocardial infarction was established. Successful preparation; (3) In infarction group, the normal myocardium was red, collagen fibers were stained green, left ventricular anterior infarction area was significantly thinned, fibrous tissue replaced normal myocardium and then formed scars, which proved the success of myocardial infarction model; (4) In infarction area, elastic fibers decreased with the extension of infarction time. Trends: The content of myocardial elastic fiber in control group was (0.97.05), 1 week after infarction (0.95.04), 2 weeks (0.22.01), 3 weeks (0.13.01), 4 weeks after infarction (0.03.004), 5 weeks after infarction (0.471.035), 1 week after infarction (0.632.045), 2 weeks (0.925.107) and 3 weeks (1.0.107), respectively. (6) With the prolongation of infarction time, the content of type III collagen increased gradually. The control group was (0.335.078), the first week after infarction (0.374.018), the second week group was (0.469.035), the third week after infarction (0.578.021) and the fourth week group was (1.134.039). Conclusion (1) The longer the infarction time, the longer the infarct area was, the longer the infarct area was, the type I collagen and type III collagen were (0.039). The remodeling of these proteins may be the pathological basis of the increased stiffness and decreased elasticity in the scar area after infarction. (2) The decrease of cardiac function is positively correlated with the decrease of elastic fibers and inversely correlated with the increase of collagen.
【学位授予单位】：新乡医学院
【学位级别】：硕士
【学位授予年份】：2017
【分类号】：R542.22

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