中文摘要：

目的观察病毒性心肌炎致死者心肌组织中血管细胞黏附分子-1（vascular cell adhesion molecule-1，VCAM-1）及半胱氨酸天冬氨酸蛋白酶-3（caspase-3）的表达及分布特点，探讨病毒性心肌炎的发病、致死机制。方法收集病毒性心肌炎致死案例20例作为实验组，交通事故致创伤性、失血性休克死亡案例10例作为对照组，取心肌组织切片进行VCAM-1及caspase-3免疫组织化学染色后显微镜下观察．经图像分析和统计学处理，比较两组染色后VCAM—l及caspase-3阳性表达的差异。结果（1）实验组VCAM-1免疫组织化学染色阳性表达呈深棕黄色，染色部位主要位于血管内皮细胞内，对照组呈微弱阳性表达。实验组平均光密度高于对照组（P〈0．05）。（2）实验组caspase-3免疫组织化学染色阳性表达为棕红色颗粒．主要位于心肌血管周围炎症细胞中，实验组阳性细胞数多于对照组（P〈0．05）。结论VCAM-1可能在病毒性心肌炎引起的炎症细胞渗出过程中发挥重要作用，可为病毒性心肌炎致死案例中的法医病理学诊断提供参考，而caspase-3介导的心肌细胞凋亡参与病毒性心肌炎晚期致死机制的作用不明显。

英文摘要：

Objective To observe the expression and distribution of vascular cell adhesion molecule-1 （VCAM-1） and caspase-3 in myocardium of persons who died from viral myocarditis and to explore its pathogenesis and death mechanism. Methods Twenty cases died from viral myocarditis were selected as the experimental group. Ten cases died from traumatic shock and massive hemorrhage shock after traffic accidents were selected as the control group. The sections of myocardium were stained by immunohisto- chemistry for VCAM-1 and caspase-3, and observed under microscope. The positive expressions of VCAM-1 and caspase-3 of the two groups were compared with each other by image analysis and statistical analy- sis. Results （1） The vascular endothelial cells expressed VCAM-1 with dark nigger-brown colors in the experimental group, and weak expression was observed in the control group. The average optical density in the experimental group was higher than that in the control group （P〈0.05）. （2） The caspase-3 posi- tive cells were mostly inflammatory cells around the myocardial vessels with brown-red granules in the experimental group. The positive cell number in the experimental group was higher than that in the con- trol group （P〈0.05）. Conclusion VCAM-1 may play an important role in the inflammatory cells exuda- tion caused by viral myocarditis, and may provide the reference for diagnosis of viral myocarditis in forensic pathology. However, the myocardial apoptosis mediated by caspase-3 doesn＇t affect the lethal mechanism in the late stage of viral myocarditis.