AIM:To investigate the effects of autoantibodies against β 1 -adrenoceptor in hepatitis virus myocarditis on action potential and L-type Ca 2+ currents.
METHODS:Fifteen samples of autoantibodies against β 1 -adrenoceptor positive sera of patients with hepatitis virus myocarditis were obtained and IgGs were purified by octanoic acid extraction. Binding of autoantibodies against β 1 -adrenoceptor to guinea pig cardiac myocytes was examined by immunofluorescence. Using the patch clamp technique, the effects on the action potential and I Ca-L of guinea pig cardiac myocytes caused by autoantibodies against β 1 -adrenoceptor in the absence and presence of metoprolol were investigated. Cell toxicity was examined by observing cell morphology and permeability of cardiac myocytes to trypan blue.
RESULTS:The specific binding of autoantibodies against β 1 -adrenoceptor to guinea pig cardiomyocytes was observed. Autoantibodies against β 1 -adrenoceptor diluted at 1:80 prolonged APD 20 , APD 50 and APD 90 by 39.2%, 29.1% and 15.2% respectively, and only by 7.2%, 5.3% and 4.1% correspondingly in the presence of 1 µmol/L metoprolol. Autoantibodies against β 1 -adrenoceptor diluted at 1:80, 1:100 and 1:120 significantly increased the I Ca-L peak current amplitude at 0 mV by 55.87±4.39%, 46.33±5.01% and 29.29±4.97% in a concentration-dependent manner. In contrast, after blocking of β 1 -adrenoceptors (1 µmol/L metoprolol), autoantibodies against β 1 -adrenoceptor diluted at 1:80 induced a slight increase of I Ca-L peak amplitude only by 6.81±1.61%. A large number of cardiac myocytes exposed to high concentrations of autoantibodies against β 1 -adrenoceptor (1:80 and 1:100) were turned into rounded cells highly permeable to trypan blue.
CONCLUSION:Autoantibodies against β 1 -adrenoceptor may result in arrhythmias and/or impairment of myocardiums in HVM, which would be mediated by the enhancement of I Ca-L .