小鼠病毒性心肌炎的心肌结构及左室功能变化的初步研究

Characteristics of morphology and left ventricular function in the mouse with myocarditis

目的 :探讨病毒性心肌炎时的心肌结构与收缩力变化的关系。方法 :建立病毒性心肌炎的动物模型 ,观测病毒损伤阶段和免疫损伤阶段心肌的超微结构和心肌收缩力改变。结果 :病毒性心肌炎早期的心肌细胞的线粒体超微结构发生了变化 ,心肌细胞收缩力下降 ,左室压 (LVP)为 (14 2± 0 8)kPa ,dp/dt为 (2 73 1±10 0 )kPa/s,正常对照LVP为 (17 1± 0 7)kPa ,dp/dt为 (35 9 8± 9 3)kPa/s,P <0 0 1;后期心肌组织严重损害 ,不仅有线粒体溶解破坏 ,而且肌原纤维变细、减少等 ,并且心肌收缩力指标明显下降 ,LVP为 (11 8± 0 2 )kPa ,dp/dt为(2 0 9 5± 6 9)kPa/s,与早期相比差异有显著 ,P <0 0 1。结论 :病毒性心肌炎早期 ,即病毒损伤期 ,造成心脏功能下降的原因主要是病毒引起心肌细胞的超微结构改变 ,特别是对线粒体的损伤 ,使心肌细胞供能障碍 ,心肌收缩力减小 ;病毒性心肌炎后期 ,免疫反应造成心肌组织损害较病毒直接损害更严重 ,造成心肌收缩力明显减小。

AIM:To determine the relationship between microhistology and cardiac contractility in myocarditis animal model. METHODS:Setting up myocarditis animal model by injecting Coxsackivevirus B 3 (CVB 3) into mice, then observed myocardial morphological changes and measured left ventricular function of mice at the time of first three days and two weeks after injecting CVB 3.RESULTS:Subcellular structure (mitochondria) changed at the first three days after injecting CVB 3. The left ventricular pressure (LVP) and the rate of intraventricular pressure development (d p /d t ) which is the index of reflecting cardiac contractility depressed in this stage (14.2±0.8) kPa and (273.1±10.0)kPa/s, respectively. There were (17.1±0.7)kPa and (359.8±9.3)kPa/s in normal mice, respectively ( P <0.01). Myocardial lesions were more severe during immune response stage-two weeks after injecting CVB 3, including myocardial inflammation and necrosis. LVP was (11.8±0.2)kPa and d p /d t was (209 5±6 1)kPa/s in immune response stage. There was significant difference between mice with myocarditis at early stage and at immune response stage ( P <0.01).CONCLUSIONS:The factor of causing the depression of cardiac contractility in early stage (virus-induced damage) is mainly change of subcellular structure. Mitochondria cannot provide energy as normal. There were more severe myocardial lesions in later stage (cell-mediated autoimmune response)than in early stage. The depression of cardiac contractility is a consequence of multifactor. 1 )kPa/sinimmuneresponsestage.Therewassig