病毒性心肌炎发病机理的实验研究──T细胞亚群和抗心肌抗体检测

Studies on the Pathogenic Mechanism of Viral Myocarditis──Assay of Lymphocyte Subsets and Anti-car diac Antibodies

以柯萨奇Ｂ＿３病毒（ＣＶＢ＿３）感染Ｂａｌｂ／ｃ小鼠建立心肌炎模型，检测了小鼠脾脏中Ｔ细胞亚群和血清中的抗心肌抗体，并进行了心脏病毒分离及组织病理学检查。结果显示，病毒感染后５天，脾脏中Ｔｈｙ１，２￣＋（Ｔ＿总）增高，７一１５天降低，第２１天恢复正常。Ｌ３Ｔ４￣＋（Ｔｃ／Ｔｓ）于病毒感染后５一２１天均明显高于对照组。Ｌ３Ｔ４＋（Ｔｈ／ｉ）于病毒感染后７天开始增高，直到２１天均明显高于对照组。病毒感染后１５天，抗心脏肌球蛋白抗休开始增高，第２１天继续增高。病毒感染后３一５天，心脏病毒分离均为阳性；第７天部分小鼠心脏中仍可分离出病毒；第１５天心脏病毒分离为阴性。病毒感染后７一２１天，心肌坏死、间质炎细胞浸润等病理变化进行性加重。上述结果提示，病毒感染本身和免疫因素都可能参与心肌炎的发病。

this study,we established myocarditis model by using coxsackie type B3 inoculation.Results of the study revealed the following:5 days after inoculation,the percentage of Thylcells in the spleen of infected mice was increased,ttien it was decreased significantly on day7,15 and 2 1,L 3T4￣+subsets were increased on days 7,15and 2 1.Anti-cardiac antibodies inthe serum of infected mice were increased after inoculation.Virus was isolated from all thehearts of infected mice on days 3 and 5.The percentage of Dositive viral isolation were de-creased on day 7.Focal necrosis appeared in the myocardium with small lymphocytes infiltra-tion on day 5.Mvocardiac necrosis and inflammatory cell infiItration became more severe onday 7. and the ventricular cavity began to dilatate on days 1 5. Capillary and fibroblast in thenecrotic area appeared on day 2 1. The above results revcaled that T lymphocyte subsets,anti-cardiac antibodies and virus itself all may be associated with viral myocarditis.