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.