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目的:探讨银杏叶提取物(Egb761)对家兔心室肌细胞瞬时外向钾电流(Ito)和动作电位的作用,揭示其抗心肌缺血及缺血引起的心律失常的离子机制。方法:酶解法分离家兔的心室肌细胞。全细胞膜片钳技术记录心肌细胞的Ito和动作电位及其被Egb761作用后的变化。结果:①在电压钳制方式下,60μg/L Egb761作用心室肌细胞5 min后,各个钳制电位下的Ito均明显增大,在钳制电位为+50 mV时,Egb761使Ito的电流密度由对照组的(7.59±0.19)pA/pF增加到(11.18±0.89)pA/pF(P<0.01,n=8),Egb761还使Ito的I-V曲线比对照组Ito的I-V明显抬高,但I-V曲线方向没有发生改变,表明Egb761引起了心肌细胞Ito的明显外流。②在电流钳制下,对照组心室肌细胞动作电位都具有从0期到4期的动作电位形态,60μg/L Egb761使心肌细胞动作电位形态呈三角形尖锥锋形,动作电位时程(APD)明显缩短,其复极化50%时程(APD50)和复极化90%时程(APD90)分别由(83.6±4.3)ms缩短为(51.3±3.2)ms和由(168.7±4.1)ms缩短为(93.8±4.4)ms(分别与对照组相比,P<0.01,n=8),尽管Egb761使动作电位幅度(APA)和静息电位(RP)降低,但与对照组相比,没有显著性差异(P>0.05)。结论:Egb761可使心室肌细胞Ito显著增加和APD明显缩短,从而减轻心肌缺血时细胞内阳离子超载对心肌造成的损伤和心肌缺血引起的心律失常的发生,以及增加心脏泵血功能。
OBJECTIVE: To investigate the effect of Ginkgo biloba extract (Egb761) on the transient outward potassium current (Ito) and action potential of rabbit ventricular myocytes, and to reveal its ion mechanism against arrhythmia induced by ischemia and ischemia. METHODS: Rabbit ventricular myocytes were isolated by enzymatic hydrolysis. Whole-cell patch clamp technique was used to record the changes of Ito and action potentials of cardiomyocytes and their action by Egb761. RESULTS: 1 Under the voltage clamping mode, the Ito under the clamped potential increased significantly after 60 μg/L Egb761 treated for 5 min. When the clamped potential was +50 mV, the current density of Ito induced by Egb761 was controlled by the control group. The (7.59±0.19)pA/pF increased to (11.18±0.89)pA/pF (P<0.01, n=8). Egb761 also increased the IV curve of Ito significantly higher than that of Ito in the control group, but the IV curve direction There was no change, indicating that Egb761 caused a significant outflow of Ito in cardiomyocytes. 2 Under current-clamping, the action potentials of the ventricular myocytes in the control group all have the action potential morphology from 0 to 4 phases, and 60μg/L Egb761 makes the action potential of cardiomyocytes have a triangular tip, and the action potential duration (APD). Significantly shortened, its repolarization 50% time course (APD50) and repolarization 90% time course (APD90) shortened from (83.6 ± 4.3) ms to (51.3 ± 3.2) ms and shortened by (168.7 ± 4.1) ms, respectively It was (93.8±4.4) ms (P<0.01, n=8, respectively, compared with the control group). Although Egb761 decreased the action potential amplitude (APA) and resting potential (RP), there was no comparison with the control group. Significant difference (P>0.05). Conclusion: Egb761 can significantly increase Ito in ventricular myocytes and significantly shorten the APD, thereby reducing the myocardial damage caused by cation overload in myocardial ischemia and the occurrence of arrhythmia caused by myocardial ischemia, and increasing the pumping function of the heart.