【摘要】 目的 研究肝炎病毒诱导的抗β1肾上腺素能受体抗体对心肌细胞L型钙电流和胞内钙的影响。方法 利用膜片钳和激光共聚焦技术观察抗β1肾上腺素能受体抗体对豚鼠心肌细胞动作电位、L型钙电流和胞内钙的影响以及美托洛尔的药物干预情况。结果 1:80抗β1肾上腺素能受体抗体分别使APD20、APD50和APD90延长39.2％、29.1％和15.2％。1:80、1:100和1:120抗β1肾上腺素能受体抗体分别使L型钙电流峰值和胞内钙荧光强度增加(55.87±4.39)％和(140.00±13.30)％、(46.33±5.01)％和(107.00±14.10)％、(29.29±4.97)％和(57.00±5.96)％,呈现浓度依赖性。该抗体致胞内钙增加与钙内流和肌浆网钙释放有关。经1μmoL/L美托洛尔预先阻断β1肾上腺素能受体后,1:80抗β1肾上腺素能受体抗体仅能使APD20、APD50和APD90延长7.2％、5.3％和4.1％,L型钙电流峰值和胞内钙荧光强度增加(6.81±1.61)％和(10.97±2.55)％。结论 肝炎病毒诱导的抗β1肾上腺素能受体抗体所介导的心肌细胞L型钙电流和胞内钙增加可能是其导致心律失常和(或)心肌损伤的机制之一。更多还原

【Abstract】 Objective To investigate the effects of autoantibodies against β1-adrenoceptors induced by hepatitis viruses on L-type Ca2+ currents and intracellular Ca2+ concentration. Method The patch clamp technique and the confocal technique were used to investigate the effects of autoantibodies against β1 -adrenoceptors in the absence and the presence of metoprolol on the action potential, L-type Ca + currents and intracellular Ca2 + concentration of guinea pig cardiac myocytes. Results 1: 80 autoantibodies against β1-adrenoceptors prolonged APD20, APD50 and APD90 by 39.2%, 29.1% and 15.2% respectively, whereas in the presence of 1 μmol/L metoprolol the prolongations were only 7. 2% , 5. 3% and 4. 1% , respectively. Autoantibodies against β1-adrenoceptors diluted at 1: 80, 1: 100 and 1: 120 significantly increased the ICa-L peak current amplitude and intracellular Ca2+ fluorescent intensity by (55. 87 ±4. 39)% and (140. 00 ±13. 30)%, (46. 33 ±5. 01)% and (107. 00 ± 14. 10)% , (29. 29 ±4. 97)% and (57.00± 5.96)%, respectively, in a concentration-dependent manner. The elevation of intracellular Ca2+ concentration was associated with Ca2 + influx and Ca2+ release in sarcoplasmic reticulum. In contrast, after blocking β1-adrenoceptors with 1 μmol/L metoprolol, autoantibodies against β1-adrenoceptors diluted at 1:80 induced the increase of ICa-L peak amplitude and intracellular Ca2+ fluorescent intensity only by (6. 81 ± 1.61)% and (10.97 ±2.55)%. Conclusion Arrhythmias and (or) the impairment of myocardiums caused by autoantibodies against β1-adrenoceptors induced by hepatitis viruses would be mediated by the enhancement of ICa-L and the elevation of intracellular Ca2 + concentration.更多还原