牛磺酸镁对缺氧/复氧致大鼠心肌细胞钙离子通道异常的影响

摘要

目的：观察牛磺酸镁配合物( taurine magnesium coordi-nation compound,TMCC)对缺氧/复氧损伤所致大鼠心室细胞异常L-型钙电流( ICa,L )的影响,以探讨其抗心律失常作用机制。方法酶解法分离大鼠单个心室肌细胞,应用全细胞膜片钳技术记录低(100μmol·L-1)、中(200μmol·L-1)、高(400μmol·L-1)3个浓度的牛磺酸镁及胺碘酮(24.24μmol·L-1)对缺氧/复氧大鼠心室细胞 ICa,L的影响。结果缺氧/复氧使大鼠心室肌细胞 ICa,L峰值从(3．35±0．50) pA/pF增大到(5．69±0．25) pA/pF(n=6, P0．05)、(4．41±0．22) pA/pF、(3．82±0．21) pA/pF(n=6, P0. 05),(4. 41 ± 0. 22) pA/pF, (3. 82 ± 0. 21)pA/pF(n=6, P<0. 01) by TMCC(100, 200, 400 μmol·L-1 ) and amidodarone 24. 24 μmol·L-1 restored peak ICa,L to(3. 66 ± 0. 27)pA/pF (n=6,P<0. 01 ) . Compared to control group, hypoxia-reoxy-genation turned ICa,L steady-state activation curves to left and inactivation curves to right, which quickened activation and slowed inactivation, TMCC ( 200, 400μmol · L-1 ) and amiodarone could restore the left shift activation curves and right shift inactivation curves. Conclusion TMCC can concentration-de-pendently restore the increase of calcium current due to hypoxia-reoxygenation by promoting inactivation process and inhibiting activation process, and the effect is equal to that of amiodarone. TMCC blocks ICa,L of the ventricular cardiomyocytes, which may be one of its antiarrhythmic mechanisms.