肌球蛋白诱导大鼠自身免疫性心肌炎不同时期心功能及心肌病理学变化

目的:观察心肌肌球蛋白诱导自身免疫性心肌炎不同时间实验大鼠心功能及心肌组织病理学动态变化。方法:以猪心肌肌球蛋白为致病性抗原,与完全弗氏佐剂等体积混合成乳浊液在实验第1天、8天、30天皮下注射免疫Lewis大鼠作为心肌炎组,以完全弗氏佐剂皮下注射大鼠作为对照组。HE染色和Masson染色观察两组大鼠初次免疫后第21天、30天、90天心肌病理变化,超声心动图检测两组大鼠初次免疫后第21天、30天、90天的射血分数(EF)、左室短轴缩短分数(FS)、左室舒张末内径(LVEDd)、左室收缩末内径(LV-EDs)及左心室后壁厚度(LVPW)等指标。结果:免疫后不同时间超声心动图检测提示心肌炎组大鼠心功能较对照组明显下降(EF:84.25±2.17%vs93.45±4.13%,P<0.05;FS:48.49±4.36%vs63.17±4.49%,P<0.05;LVEDd:3.66±0.35mmvs4.63±0.32mm,P<0.05)。免疫后第21天,HE染色见心肌炎组大鼠心肌细胞肿胀、变性、坏死及不同程度的急性炎性细胞浸润,至第90天心肌组织炎症减弱,间质出现纤维化,胶原容积分数升高,对照组大鼠未出现心肌炎症及纤维化。结论:心肌肌球蛋白可诱导大鼠实验性自身免疫性心肌炎,急性期心功能受损主要由心肌炎症引起,慢性期病理学改变主要表现为心肌纤维化。

Change of Heart Function and Myocardial Histopathology in Different Periods of Autoimmune Myocarditis in Rats Immunized with Cardiac Myosin

Objective:To observe the sequential change of heart function and myocardial histopathology in different periods of autoimmune myocarditis in rats immunized with cardiac myosin.Method:Cardiac myosin was pathogenic antigen.Lewis rats of the myocarditis group were immunized with cardiac myosin covered by complete freund's adjuvant(CFA)on the 1st,8th,30th day.The control rats were immunized with CFA only.On the 21st,30th and 90th day after primary immunization,HE and Massine trichrome staining were used to identify the myocardial pathological changes in rats of two groups.Echocardiography were used to examine the left ventricular ejection fraction(EF),the left ventricular fractional shortening score(FS),the left ventricular end diastolic diameter(LVEDd),the left ventricular end systolic diameter(LVEDs)and left ventricular posterior wall thickness(LVPW)and so on.Results:The different time after immunization,echocardiography detected prompts myocarditis rats decreased heart function(EF:84.25±2.17% vs 93.45±4.13%,P<0.05;FS:48.49±4.36% vs 63.17±4.49%,P<0.05;LVEDd:3.66±0.35 mm vs 4.63±0.32 mm,P<0.05).On the 21st day,histopathological examination of cardiac tissue showed an obvious inflammatory cell infiltrate with myocyte necrosis in myocarditis group;on the 90th day,inflammation diminished,interstitial fibrosis occured and collagen volume fraction increased.No inflammation and fibrosis was emerged in the myocardium of control rats.Conclusion:The cardiac myosin can induce rat experimental autoimmune myocarditis(EAM);the acute phase of cardiac function impaired by myocarditis,and the histopathological changes in chronic phase was mainly expressed in myocardial fibrosis.