CAJ | 학술논문

目的　建立柯萨奇B3m（Cox B3m）病毒性心肌病变模型，用原位PCR方法检测心肌病变中的病原，以阐明Cox B3m病毒在发病过程中的作用。方法　(1)用Balb/C小鼠30只，制作Cox B3m病毒性急性心肌病变模型，50只制作慢性反复感染心肌病变的动物模型；并与25只正常Balb/C小鼠相对照；(2)对病毒反复感染所致慢性心肌病变动物模型的左室侧壁厚度及左室腔的面积大小，采用KS400型图像分析系统进行图像分析；(3)应用碱性磷酸酶联接的抗地高辛抗体标记的核苷酸直接掺入法建立原位PCR检测心肌组织中柯萨奇B3m病毒RNA。结果　不论是在急性或反复感染的慢性心肌病变模型心肌组织中100%可找到CVB-RNA阳性信号，慢性病变者经图像分析证明左心腔扩大，室壁变薄，与正常对照组相比P<0.01～<0.05。结论　在病变心肌组织中，用原位PCR检测都有阳性的CVB-RNA信号, 说明柯萨奇B3m病毒不仅能引起急性病变, 反复感染者亦可造成慢性病变, 后者心腔常扩大且室壁变薄。
목적　건립가살기B3m（Cox B3m）병독성심기병변모형，용원위PCR방법검측심기병변중적병원，이천명Cox B3m병독재발병과정중적작용。방법　(1)용Balb/C소서30지，제작Cox B3m병독성급성심기병변모형，50지제작만성반복감염심기병변적동물모형；병여25지정상Balb/C소서상대조；(2)대병독반복감염소치만성심기병변동물모형적좌실측벽후도급좌실강적면적대소，채용KS400형도상분석계통진행도상분석；(3)응용감성린산매련접적항지고신항체표기적핵감산직접참입법건립원위PCR검측심기조직중가살기B3m병독RNA。결과　불론시재급성혹반복감염적만성심기병변모형심기조직중100%가조도CVB-RNA양성신호，만성병변자경도상분석증명좌심강확대，실벽변박，여정상대조조상비P<0.01～<0.05。결론　재병변심기조직중，용원위PCR검측도유양성적CVB-RNA신호, 설명가살기B3m병독불부능인기급성병변, 반복감염자역가조성만성병변, 후자심강상확대차실벽변박。
Objective　To detect the location of pathogens in myocardium using in situ RT-PCR technique in order to study the pathogenetic course of the myocardial lesion induced by CoxB3m virus infection in mice. Methods　(1) Thirty and fifty Balb/c mice were used respectively to establish the acute and chronic CoxB3m infected models, with another 25 healthy mice as the controls; (2) KS400 image analysis system (Germany) was used to measure the cardiac chamber area and the left ventricular wall thickness of the chronic infected mice and the controls; (3) CoxB3m virus in myocardial tissue was detected using in situ RT-PCR by direct incorporated technique which employed nucleotide labeling by anti-digoxin antibody and bonded with alkaline phosphatase (anti-dig-AKP method). Results　Picture analysis indicated that the left ventricular chamber area was enlarged and the left ventricular wall was thinner in the chronic repeated virus infected models than those of the controls. With in situ RT-PCR, positive signals for Coxsackie virus B3m RNA were detected not only in the myocardium of the acute Balb/c mice models but also in the myocardium of the chronic mice models. Conclusion　Coxsackie virus B3m is able to induce pathologic lesions by exhibiting positive CVB-RNA signals in both acute and chronic models in mice. In the chronic experimental models, the cardiac chamber is enlarged while the ventricular wall is thinned which demonstrates the association with persistent infection of Coxsackie virus B3m virus.