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柯萨奇B3病毒诱导鼠心肌炎血浆β-内啡肽及其受体的变化
徐玉莲,丁继军,沈茜
0
()
摘要:
目的:观察病毒性心肌炎病理过程中内源性阿片系统激活的动态变化,探讨阿片肽在心肌炎病理损伤中的作用。方法:以柯萨奇B3病毒(Cox B3)诱导BALB/c鼠心肌炎为实验模型,观察感染后第3,7 ,10,15,25和35 d鼠体、肝和肺的质量,血浆β-内啡肽(β-EP)水平、心肌细胞膜 β-EP受体及心肌病损程度。采用放射免疫法测定血浆 β-EP、放射配体结合法测定 β-EP受体、常规病理检查心肌病损程度。结果:以1 000 TCID50Cox B3感染BALB/c鼠,约92.8%(65-70)鼠诱导出典型的心肌炎病理改变。感染后3-25 d受染鼠血浆 β-EP水平显著高于正常对照组;感染后10-25 d受染鼠肺/体质量和肝/体质量比均高于正常对照鼠,提示受染鼠出现较严重的充血性心力衰竭。同时,受染鼠心肌细胞膜 β-EP受体Bmax显著增高,Kd值变化不明显。结论:由于病毒和自身免疫对心肌细胞的损伤,使病毒性心肌炎患鼠出现充血性心力衰竭,引起循环中阿片肽水平升高及相应受体的变化。通过神经内分泌-免疫网络,这些变化必将对心脏的病理损伤产生明显的作用。
关键词:  柯萨奇病毒B组、心肌炎、内啡肽类
DOI:
基金项目:
The changes of plasma β-Endorphin level and its receptor in cardiac myocyte in murine coxsackievirus B3 induced myocarditis
徐玉莲,丁继军,沈茜
()
Abstract:
Objective:To observe the kinetics of endogenuous opiate system activation and study the roles of opiate polypeptides in the pathogenesis of immunoinjury in virul myocarditis. Methods: Balb/c mice with myocarditis induced by 103 TCID50 coxsackie B3 virus were used as experimental model. Plasma β endorphin levels were determined by radioimmunoassay, endorphin receptor on membrane of cardiac myocyte were measured with radioligand binding technique, cardiac pathology and organ mass (heart,lung) were observed at days 3,7,10,15,25 and 35 after infection. Results:Infection with 103 TCID50 coxsackie B3 virus produced a classic pathological picture of myocarditis in 92.8%(65/70) infected mice. Plasma endorphin concentration was significantly increased at days 3 to 25 postinfection compared to the normal controls. The ratios of liver mass and lung mass to body mass were obviously greater at days 10 to 25 after infection in myocarditis animals than in normal animals, the results might reflect more severe congective heart failure caused by myocardial damage in myocarditis animals. Simultaneously, the increase of binding for endorphin on membrane of cardiac myocytes were detected, but the change in the Kd of receptor were not found in myocarditis mice. Conclusion:The endogenous opiate system is activated in congestive heart failure caused by myocardial damage in murine coxsackievirus B3 my ocarditis, which might affect the cardiac pathogenesis because of the neuroimmunoical modulating effects by opiate polypeptides.
Key words:  coxsackie B virus  myocarditis  endorphins