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作 者:杨英珍[1] 金佩英[1] 郭棋[1] 杨学义[1] 浦寿月[1] 陈灏珠[1] 杨俊华[2] 王克强[3] 施建英[2] 龚祖埙[4] 沈菊英[4] 彭宝珍[4]
机构地区:[1]上海医科大学附属中山医院上海市心血管病研究所 [2]上海医科大学病理教研室 [3]上海医科大学解剖教研室,上海 [4]中国科学院上海生物化学研究所
出 处:《病毒学杂志》1989年第3期233-238,共6页
摘 要:小鼠感染Coxsackie B-3病毒后7天,各鼠心脏均出现巨检病变,组织学检查心肌细胞示变性、坏死及炎性细胞浸润,心肌切片作图象分析示病灶总面积/所测心肌总面积为11.3%,并有明显心肌超微结构改变。心肌中分离到病毒。对照鼠心脏均无上述改变,亦未分离到病毒。本模型可作为进一步探索病毒性心肌炎药物治疗的基础。An experimental acute myocarditis caused hy Coxsaekie B-3 virus(CB_3V)was developed in male BALB/c mice 4 weeks of age. The animals were szc-rificed at the 7th day after infection, After gross examination, the heart was cut transversely into 3 pieces for light, electron microscopic examinations andvirus assay. In addition, myocardial lesions were also quantitatively measuredby image analysis. White spots, streaks or patches were seen on the surface of ventrieles ofhearts in the infected group (14 mice) .The myocardial lesions included dege-neration, necrosis, lymphoeyte and mononuclear cell infiltration in the inters-titum. Mitochondria showed rupture of membrane, enlargement of internal vac-ant space and indistinctness of the structure. In severe lesions, there were fra-gmented myofibers, distended myocardial T tubes, dilated sarcoplasmic reticulaand unintegral mitochondria. The total lesion area and total deteeted myocar-dial area were 9.6 mm^2 and 84.64 mm^2, respectively (total 8 slices). Briefly,the total lesion area/total detected myocardial area was 11.3%. CB_3V was iso-lated from the infected myocardium and the virus titer was 5.19±2.08(1gTCID_(50)). No heart lesions were found and no virus was isolated from 12uninfected mice. The experimental myocarditis model would be useful for studying the ef-fect of some drugs on acute viral myocarditis.
分 类 号:R373.23[医药卫生—病原生物学]
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