| Background Acute myocardial infarction(Acute myocardiac infarction,AMI)is a common and frequently-occurring disease which seriously hazard to human health.After AMI,the infarction area is gradually replaced by the scar tissue,seriously affecting heart function,and even leading to heart failure.In disease condition changes may occur throughout the myocardial infarction area,not only in myocardial cells,but significant changes may also occur in a variety of ingredients in the intercellular substance,especially in collagen fibers and elastic fibers.At present,changes of the myocardial cells and the neogenesis of capillaries after AMI receive more attention,but research focus on dynamic changes of collagen fiber and elastic fiber in myocardial interstitial and their relationship with cardiac function receive much less attention.Therefore,this study intends to explore dynamic changes of type I collagen fiber,type III collagen fiber and elastic fibers in infarction scar tissue at different weeks after acute myocardial infarction and their relationship with the cardiac function,aiming to provide a new research idea for myocardial regeneration,and also provide experimental basis and theory reference for clinical treatment after AMI.Objective This study intends to explore dynamic changes of type I collagen fiber,type III collagen fiber and elastic fibers in infarction scar tissue at different weeks after acute myocardial infarction and their relationship with the cardiac function,aiming to provide a new research idea for myocardial regeneration,and also provide experimental basis and theory reference for clinical treatment after AMI.Methods(1)50 SD rats were randomly divided into control group(n = 10)and experimental group(n = 40).The left coronary artery was not ligated in the control group,and acute myocardiac infarction(AMI)model was established with Sprague-Dawley rats by ligation of the left anterior descending coronary artery;(2)B ultrasonic instrument of the prison for small animals monitors cardiac function changes,and pathological changes of the model were detected by Masson staining.(3)The dynamic changes of collagen I,collagen III and elastic fiber expression were detected by immunohistochemistry,Immunofluorescence and Western blotting at infarct region in the heart of rats at 1 week,2 weeks,3 weeks,and 4 weeks after AMI.Results(1)After the left anterior descending coronary artery was ligated,the myocardium below the ligation were turned into purple or pale,and the left auricle congested heart beat weakened.AMI was diagnosed using EKG,showing II ST segment of the infarction group 20 minutes after ligation shifted,leading to an ST segment arch upward-push by about 0.2 m V,showing that the ligature was successful and also indicates that the myocardial infarction model was successfully established.(2)Compared with the control group(74.90% ± 4.13),the cardiac function in the model rats were gradually decreased.The first week(58.00% ± 2.38),second week(51.74% ±2.16),third week(37.50% ± 3.00)and at the 4th week were(28.92% ± 2.83).LVEF,LVFS and IVS were also gradually decreased,but LVIDs and LVIDd increased with post AMI time compared with normal heart,demonstrating impairment of heart function.In addition,cardiac function was gradually decreased with time,especially 2-3 weeks after infarction.Myocardial infarction models were successfully established and LVPW did not change therein.(3)Taking the infarction group,sections,after being paraffin-embedded were Masson stained to show that undamaged heart tissue was presented as red,but AMI damaged heart was blue due to collagen fibres replacement.The front wall of the left ventricle was significantly thinner,infarcted myocardial tissue was replaced by fibrous scar tissue,demonstrating of the myocardial infarction models.(4)Elastin was decreased gradually,it was 0.97±0.05 in the control heart,but were0.95±0.04,0.22±0.01,0.13±0.01,or 0.03±0.004,respectively at the weeks 1,2,3 or 4 in the AMI heart.(5)Production of COLI was increased gradually with AMI time;the normal group was(0.471±0.035),and for the infarction groups were as follows 1 week(0.632±0.045),2weeks(0.925±0.107),3 weeks(1.071±0.099),and 4 weeks(1.114±0.057).(6)With the extension of infarction time,collagen III content increasing,the normal group were(0.354±0.078),the normal group was(0.335±0.078),and for the infarction groups were as follows 1 week(0.374±0.018,2 weeks(0.469±0.035),3 weeks(0.578±0.021)and 4 weeks(1.134±0.039).Conclusions(1)With the extension of time after myocardial infarction,the content of collagen I and collagen III in infarction area increased progressively,and elastic fiber decreased little by little,the reconstruction of these proteins may be the pathological foundation which leaded to resilience lowered and stiffness augmented in scar area after infarction.(2)Reduced cardiac function was proportional to the decrease of elastic fiber,and inversely proportional to the accumulation of collagen fiber. |
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