【摘要】：背景急性心肌梗死(Acute myocardiac infarction,AMI)是一種嚴重危害人類健康的高風險臨床常見病。AMI后梗死區(qū)域逐漸被瘢痕組織所替代,嚴重影響心功能,甚至出現心力衰竭。在整個心肌梗死區(qū)域變化過程中,不僅心肌細胞發(fā)生變化,細胞間質中的各種成分尤其是間質中的膠原纖維和彈力纖維均發(fā)生了重大改變。目前對心肌梗死后心肌細胞的變化和毛細血管的新生研究較多,有關心肌間質中彈性纖維和膠原纖維的動態(tài)變化及其與心功能變化的關系研究較少。目的探討大鼠急性心肌梗死后,梗死區(qū)域瘢痕組織細胞間質中I型膠原纖維、III型膠原纖維和彈力纖維不同周次的動態(tài)變化以及和心功能的關系,旨在為臨床心肌梗死后再生提供新的研究思路,為心肌梗死后的臨床治療提供實驗證據和理論參考。方法(1)隨機將50只SD大鼠分為兩組,其中對照組10只,實驗組40只。對照組開胸暴露心臟后,為了降低影響只穿線不結扎冠狀動脈左前降支,實驗組則通過將冠狀動脈前降支結扎來制備大鼠心肌梗死模型,術中通過小動物心電圖初步檢測梗死模型制備情況;(2)小動物B超儀監(jiān)測每周兩組大鼠心功能的動態(tài)變化,組織切片,Masson染色檢測模型的病理變化;(3)免疫組織化學、免疫熒光和Western Blotting技術檢測I型膠原纖維、III型膠原纖維和彈力纖維在對照組和梗死后1周、2周、3周和4周心肌梗死區(qū)域的動態(tài)變化。結果(1)術中可以看到,結扎左冠狀動脈前降支后,結扎點以下部位的心肌呈現青紫色或灰白色,左心耳充血明顯,心臟搏動減弱;與對照組對比,梗死組結扎后20分鐘心電圖II導聯ST段顯著移位,呈現出ST段弓背型向上抬高約0.2m V,說明術中結扎成功,心梗模型初步建立;(2)對照組和實驗組梗死后1周、2周、3周和4周的心功能對比顯示,實驗組模型大鼠心功能呈現下降趨勢:對照組大鼠心功能為(74.90%±4.13),實驗組梗死后第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)。且隨著梗死周次的增加,LVFS、IVS均逐漸降低,LVIDd、LVIDs逐漸增大,但LVWP變化沒有規(guī)律。表明心功能受損,且隨著梗死周次的增加,心功能逐漸降低,2-3周降低最明顯,提示心肌梗死模型制備成功;(3)梗死組各周次組織切片顯示,正常心肌呈現紅色,膠原纖維被染成綠色,左心室的前壁梗死區(qū)明顯變薄,纖維組織代替正常心肌進而形成瘢痕,證明心肌梗死模型制備成功;(4)在心肌梗死區(qū)域,隨梗死時間延長,彈力纖維呈遞減趨勢:對照組心肌彈力纖維含量為(0.97±0.05),梗死后1周為(0.95±0.04),第2周為(0.22±0.01),第3周為(0.13±0.01),梗死后4周組為(0.03±0.004);(5)I型膠原纖維含量逐漸增加,對照組為(0.471±0.035),梗死后第1周(0.632±0.045),2周組為(0.925±0.107),第3周為(1.071±0.099),4周組為(1.114±0.057);(6)隨梗死時間延長,III型膠原含量逐漸增加,對照組為(0.335±0.078),梗死后第1周(0.374±0.018),2周組為(0.469±0.035),梗死3周(0.578±0.021),第4周組為(1.134±0.039)。結論(1)心肌梗死后,時間越長,梗死區(qū)域I型和III型膠原纖維含量逐漸增多,而彈力纖維成分逐漸下降,這些蛋白的重構可能是梗死后瘢痕區(qū)域僵硬度增加、彈性下降的病理學基礎。(2)心功能的降低與彈性纖維減少正相關,與膠原的增加反相關。
[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.
【學位授予單位】：新鄉(xiāng)醫(yī)學院
【學位級別】：碩士
【學位授予年份】：2017
【分類號】：R542.22

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