CAJ | 학술논문

目的：观察牛磺酸镁配合物( taurine-magnesium coordi-nation compound,TMCC)对缺氧/复氧损伤所导致的大鼠心肌细胞异常钠通道电流的影响。方法采用Langendorff逆行主动脉灌流酶溶液消化法,急性分离大鼠单个心肌细胞,以缺氧钠外液模拟缺氧15 min后,给予有氧钠外液5 min制备缺氧/复氧模型。应用全细胞膜片钳技术,在电压钳模式下,以胺碘酮为阳性对照药,记录不同浓度TMCC对正常细胞和缺氧复氧模型细胞钠离子通道电流INa的影响。结果与正常对照组INa峰值(56．89±2．07) pA/pF相比,缺氧/复氧使大鼠心室肌细胞INa峰值减小至(35．05±1．52) pA/pF (n=6,P<0．01),I-V曲线上移。 TMCC(100、200、400μmol ·L-1)可使减小的电流呈浓度依赖性增加,分别恢复至(35．78±1．95) pA/pF (n =6,P >0．05)、(41．52±0．86) pA/pF(n=6,P<0．01)、(48．34±0．99) pA/pF(n=6,P<0．01),24．24μmol·L-1胺碘酮使其恢复为(39．44±1．24)pA/pF(n=6,P<0．01)。 TMCC和胺碘酮均能使上移的I-V曲线下移。此外, TMCC和胺碘酮还可恢复因缺氧/复氧右移的失活曲线,使失活减慢,但对激活的影响并不明显。结论 TMCC(200、400μmol·L-1)通过抑制钠通道的失活过程以恢复缺氧/复氧损伤引起的INa峰值减小,使上移的I-V曲线下移,提示该作用可能是TMCC抗缺血性心律失常的机制之一。
목적：관찰우광산미배합물( taurine-magnesium coordi-nation compound,TMCC)대결양/복양손상소도치적대서심기세포이상납통도전류적영향。방법채용Langendorff역행주동맥관류매용액소화법,급성분리대서단개심기세포,이결양납외액모의결양15 min후,급여유양납외액5 min제비결양/복양모형。응용전세포막편겸기술,재전압겸모식하,이알전동위양성대조약,기록불동농도TMCC대정상세포화결양복양모형세포납리자통도전류INa적영향。결과여정상대조조INa봉치(56．89±2．07) pA/pF상비,결양/복양사대서심실기세포INa봉치감소지(35．05±1．52) pA/pF (n=6,P<0．01),I-V곡선상이。 TMCC(100、200、400μmol ·L-1)가사감소적전류정농도의뢰성증가,분별회복지(35．78±1．95) pA/pF (n =6,P >0．05)、(41．52±0．86) pA/pF(n=6,P<0．01)、(48．34±0．99) pA/pF(n=6,P<0．01),24．24μmol·L-1알전동사기회복위(39．44±1．24)pA/pF(n=6,P<0．01)。 TMCC화알전동균능사상이적I-V곡선하이。차외, TMCC화알전동환가회복인결양/복양우이적실활곡선,사실활감만,단대격활적영향병불명현。결론 TMCC(200、400μmol·L-1)통과억제납통도적실활과정이회복결양/복양손상인기적INa봉치감소,사상이적I-V곡선하이,제시해작용가능시TMCC항결혈성심률실상적궤제지일。
Aim To investigate the antiarrhythmic mechanism of taurine-magnesium coordination com-pound on abnormal sodium current channel ( INa ) in-duced by hypoxia-reoxygenation in ventricular myocytes of rats. Methods Single ventricular myocytes were i-solated from each rat heart using enzymatic dissociation through Langendorff retrograde aortic perfusion. Whole-cell patch clamp was applied in voltage clamp mode to record INa both in normal ventricular myocytes and single ventricular myocytes of arrhythmia induced by hypoxia-reoxygenation. Results The peak density of INa was changed from ( 56. 89 ± 2. 07 ) pA/pF to (35. 05 ± 1. 52) pA/pF( n=6, P <0. 01 vs control) by hypoxia-reoxygenation with the INa I-V curve shifting upward. TMCC(200, 400 μmol·L-1)was able to re-store the reduction caused by H/R to (35. 78 ± 1. 95) pA/pF, (41. 52 ± 0. 86) pA/pF, (n=6,P <0. 01) and (48. 34 ± 0. 99) pA/pF(n=6,P<0. 01) respec-tively, but not at 100 μmol·L-1(n=6, P>0. 05), in a concentration-dependent manner, while amioda-rone restored it to (39. 44 ± 1. 24) pA/pF (n=6,P<0. 01 ) . Both high concentration of TMCC and amioda-rone could shift the I-V curve downward. In addition, TMCC and amiodarone could restore the INa inactivation curve and slow down its inactivation, whereas the acti-vation curves showed no significant differences among groups. Conclusion TMCC(200,400 μmol·L-1) could restore the H/R induced INa reduction and shift the I-V curve downward by inhibiting steady-state inac-tivation, which is suggested to be one of the mecha-nisms of the antiarrhythmic effects of TMCC in hypoxia-reoxygenation model.