Effects of autoantibodies against beta(1)-adrenoceptor in hepatitis virus myocarditis on action potential and L-type Ca(2+) currents.

Abstract:

AIM:To investigate the effects of autoantibodies against beta(1)-adrenoceptor in hepatitis virus myocarditis on action potential and L-type Ca(2+) currents. METHODS:Fifteen samples of autoantibodies against beta(1)-adrenoceptor positive sera of patients with hepatitis virus myocarditis were obtained and IgGs were purified by octanoic acid extraction. Binding of autoantibodies against beta(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 beta(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 beta(1)-adrenoceptor to guinea pig cardiomyocytes was observed. Autoantibodies against beta(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 micromol/L metoprolol. Autoantibodies against beta(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 beta(1)-adrenoceptors (1 micromol/L metoprolol), autoantibodies against beta(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 beta(1)-adrenoceptor (1:80 and 1:100) were turned into rounded cells highly permeable to trypan blue. CONCLUSION:Autoantibodies against beta(1)-adrenoceptor may result in arrhythmias and/or impairment of myocardiums in HVM, which would be mediated by the enhancement of I(Ca-L).

journal_name

World J Gastroenterol

authors

Liu K,Liao YH,Wang ZH,Li SL,Wang M,Zeng LL,Tang M

doi

10.3748/wjg.v10.i8.1171

keywords:

subject

Has Abstract

pub_date

2004-04-15 00:00:00

pages

1171-5

issue

8

eissn

1007-9327

issn

2219-2840

journal_volume

10

pub_type

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