Effects of naloxone, an opiate receptor antagonist, on coxsackievirus B3 myocarditis in the mouse.

OBJECTIVE

The aim was to test the therapeutic efficacy of naloxone, an opiate receptor antagonist, upon murine coxsackievirus B3 myocarditis with the analysis of neurohumoral kinetics.

METHODS

Two week old C3H/He mice were inoculated with 10(3) plaque forming units of coxsackie B3 virus. Naloxone, 1 mg.kg-1.d-1, was given intraperitoneally daily on days 0-14 in experiment I, and on days 14-28 in experiment II. The treated groups were compared to infected controls in each experiment. For the analysis of the endogenous opiate and neurohumoral system, plasma beta endorphin and catecholamines were measured.

RESULTS

In experiment I, survival rate did not differ significantly between naloxone treated and untreated groups (11/15 v 8/15, p = NS). Pathological scores (infiltration and necrosis), myocardial virus titres, and plasma beta endorphin and catecholamine concentrations did not differ significantly between the two groups. In experiment II, survival rate (13/16 v 6/14, P < 0.05) was higher and cardiac pathology was less severe, with a lower incidence of congestive heart failure, in naloxone than in controls groups. In addition, beta endorphin and noradrenaline were significantly increased in the naloxone group compared to the control.

CONCLUSIONS

The endogenous opiate system is activated in congestive heart failure caused by severe myocardial damage in murine coxsackie B3 myocarditis, where an associated limitation of the sympathetic system may be present. Naloxone is beneficial in congestive heart failure caused by coxsackie B3 myocarditis because of its neurohumoral modulating effect.