AIM:To investigate the effects of autoantibodies againstβ_1-adrenoceptor in hepatitis virus myocarditis on actionpotential and L-type Ca~(2+) currents.METHODS:Fifteen samples of autoantibodies against β_1-adrenoceptor positive sera of patients with hepatitis virusmyocarditis were obtained and IgGs were purified by octanoicacid extraction.Binding of autoantibodies against β_1-adrenoceptor to guinea pig cardiac myocytes was examinedby immunofluorescence.Using the patch clamp technique,the effects on the action potential and I_(ca-L) of guinea pig cardiacmyocytes caused by autoantibodies against β_1-adrenoceptorin the absence and presence of metoprolol were investigated.Cell toxicity was examined by observing cell morphologyand permeability of cardiac myocytes to trypan blue.RESULTS:The specific binding of autoantibodies againstβ_1-adrenoceptor to guinea pig cardiomyocytes was observed.Autoantibodies against β_1-adrenoceptor diluted at 1:80prolonged APO_(20),APD_(50)and APD_(90) by 39.2%,29.1% and15.2% 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 currentamplitude at 0 mV by 55.87±4.39%,46.33±5.01% and29.29±4.97% in a concentration-dependent manner.Incontrast,after blocking of β_1-adrenoceptors (1 μmol/Lmetoprolol),autoantibodies against β_1-adrenoceptor dilutedat 1:80 induced a slight increase of I_(ca-L) peak amplitude onlyby 6.81±1.61%.A large number of cardiac myocytes exposedto high concentrations of autoantibodies against β_1-adrenoceptor (1:80 and 1:100) were turned into roundedcells highly permeable to trypan blue.CONCLUSION:Autoantibodies against β_1-adrenoceptor mayresult in arrhythmias and/or impairment of myocardiums inHVM,which would be mediated by the enhancement of I_(ca-L. 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 cardiacmyocytes caused by autoantibodies against β_1 -adrenoceptorin 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 protected APO_ (20), APD_ (50) and APD_ (90) by 39.2%, 29.1% and15.2% respectively, and only by 7.2%, 5.3% and 4.1% correspondingly in presence of 1 μmol / L metoprolol. Autoantibodies against β_1-adrenoceptor diluted at 1:80, 1: 100 and 1: 120 significantly increased I_ (ca-1) 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.Incontrast, after blocking of β_1-adrenoceptors (1 μmol / A large number of cardiac myocytes exposed to high concentrations of autoantibodies against β_1-adrenoceptor (1:80), a autoantibodies against β_1-adrenoceptor dilutedat 1:80 induced a slight increase of I_ (ca_L) peak amplitude only by 6.81 ± 1.61% and 1: 100) were turned into rounded cells highly permeable to trypan blue. CONCLUSION: Autoantibodies against β_1-adrenoceptor mayresult in arrhythmias and / or impair of myocardiums in HVM, which would be mediated by the enhancement of I_ (ca-L.