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病毒性心肌炎急性期预防性干预心脏间质纤维化的实验研究
作者姓名:Jing Z  Cheng X  Yang Y
作者单位:中国医学科学院中国协和医科大学阜外心血管病医院心血管病研究所心脏肺循环研究室,上海医科大学卫生部病毒性心脏病重点实验室,中国医学科学院中国协和医科大学基础医学院
摘    要:目的探讨在病毒性心肌炎急性期预防性干预心脏间质纤维化的可行性,为明确临床干预病毒性心肌炎心脏间质纤维化的最佳时期提供实验依据。方法动物分心肌炎组、Losartan(洛沙坦)干预组、正常对照组,比较各组动物的病死率;HE染色及苦味酸天狼猩红胶原特异染色偏振光显像观察心脏间质中I型、II型胶原的表达,并半定量分析;通过阻抗微分法观察心排血量并计算心指数来评价心功能。结果Losartan干预后的心肌炎小鼠病死率为75.0%,明显高于无药物干预组41.7%,存活小鼠的心指数:药物干预组为0014±0001ml·min-1·cm2,心肌炎组和正常对照组分别为0019±0004ml·min-1·cm2、0024±0002ml·min-1·cm2,药物干预组胶原的扫描面积积分为21±08mm,心肌炎组和正常对照组分别为47±22mm、37±15mm。结论病毒性心肌炎急性期胶原已经增生,但其作用是修复坏死的心肌,Losartan能破坏此过程使心功能进一步恶化,加重病情发展,不能把急性期作为干预心肌纤维化的合适时期。

关 键 词:心肌炎  胶原

Preventional intervention of myocardial interstitial fibrosis in murine myocardium with acute myocarditis
Jing Z,Cheng X,Yang Y.Preventional intervention of myocardial interstitial fibrosis in murine myocardium with acute myocarditis[J].National Medical Journal of China,1998,78(9):699-701.
Authors:Jing Z  Cheng X  Yang Y
Institution:Division of Cardio-Pulmonary Circulation, Fuwai Heart Hospital & Institute of Cardiovascular Disease, PUMC & CAMS, Beijing.
Abstract:OBJECTIVES: To explore that whether intervening the fibrosis of heart interstitium in acute viral myocarditis is practical or not, and offer the experimental basis for clinic to choose the optimum period to intervene myocardial fibrosis. METHODS: Animals were divided into three groups: myocarditis, myocarditis intervened by Losartan, and normal control. The death rate of every group was compared. HE staining and picrosirius red staining and circularly polarized light were used to investigate myocardial collagen expression. Cardiac output was measured by impedance differentiation, and cardiac index was computed to evaluate cardiac function. RESULTS: The death rate of the group with Losartan was 75.0%, and that of the myocarditis group was 41.7%. The cardiac index of the group with the drug was 0.014 +/- 0.001 ml.min-1.cm2, the myocarditis group 0.019 +/- 0.004 ml.min-1.cm2, and the normal control 0.024 +/- 0.002 ml.min-1.cm2. The scanning area of collagen in the group with the drug was 2.06 +/- 0.77 mm, the myocarditis group 4.72 +/- 2.22 mm and the normal control 3.74 +/- 1.50 mm. CONCLUSIONS: Collagen has increased in acute viral myocarditis, but its main role in this time is to repair the necrotic myocardium, and Losartan may block this process and make lesions develop. Therefore, the acute stage is not an practical period for intervening myocardial fibrosis in viral myocarditis.
Keywords:Viral myocarditis    Collagen  
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