益气复脉合剂治疗室性期前收缩作用机制的实验研究
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摘要
室性期前收缩的主要发病机制为心室肌由于病变具有异常自律性,且自律性绝对或相对的超过了窦房结时,他们会发出异位冲动,取而代之的控制心脏的活动,产生期前收缩。抗心律失常药物通过影响心肌细胞膜的离子通道,改变离子流,从而使心肌细胞的电生理特性改变,抑制异位起搏点的自律性,终止折返激动,抑制后除极及触发激动,起到抗心律失常的作用。但目前西医抗心律失常药物均有潜在的致心律失常作用,在治疗上存在一定的局限性。
中医药在室性期前收缩的治疗上显示了一定优势,既往文献报道单味中药存在不同的抗心律失常机制。临床上心悸患者多为虚实夹杂证,其病机多为气虚血瘀,痰瘀互阻,益气复脉合剂(原复律通脉合剂)具有益气活血,祛痰安神功效,且临床应用有效。因此,本研究意在评价益气复脉合剂抗室性期前收缩整体疗效,阐述其抗心律失常作用机制,为临床治疗提供更加完整、可靠的数据支持。
目的
采用乌头碱、氯化钙及异丙肾上腺素致心律失常经典模型的方法,利用小动物心电遥测技术,评价益气复脉合剂对室性期前收缩作用的在体疗效；利用膜片钳技术,记录益气复脉合剂对心肌细胞动作电位的影响,进一步阐述其抗心律失常作用机制,为临床治疗提供更加完整、可靠的数据支持。
方法
采用乌头碱、氯化钙致心律失常模型,随机分为空白对照组、益气复脉合剂(低、中、高剂量)组。由股静脉恒速泵入乌头碱溶液或氯化钙溶液,记录室性期前收缩(PVBs)、室性心动过速(VT)、室颤(VF)及心脏停搏(CA)和心律失常(Arrhythmia)出现时间,计算室性期前收缩(PVBs).室性心动过速(VT)、室颤(VF)的发生率及乌头碱、氯化钙用量。采用异丙肾诱发SHR大鼠心律失常模型,利用心电遥测技术,对空白对照组和中药组动物记录是否出现单发室性期前收缩(Single PVBs, SP),成对室性期前收缩(Paired PVBs, PP),室性心动过速(VT),并统计其发生率(SPR. PPR.VTR)、出现个数及出现时间。综合评价益气复脉合剂的抗心律失常作用。采用胶原酶法急性分离大鼠左心室肌细胞,利用膜片钳技术,记录心室肌细胞动作电位相关指标,探讨益气复脉合剂抗心律失常机制。
结果
1.与空白对照组比较,中药低、中、高剂量组可明显延迟乌头碱致PVBs、 VT及VF出现时间(P<0.05,P<0.01,P<0.01),并明显增加VT出现时乌头碱用量(P<0.05,P<0.01,P<0.01)；中药中、高剂量组还可显著延迟乌头碱致CA出现时间(P<0.01),并明显增加PVBs、 VF及CA出现时乌头碱用量(P<0.01)。中药不同剂量组间比较,与中药低剂量组比较,中药中、高剂量组可显著延迟PVBs.VT及VF出现时间(P<0.01),且能明显延迟CA出现时间(P<0.05,P<0.01),并可显著增加PVBS、 VT, VF及CA出现时乌头碱用量(P<0.01)。说明益气复脉合剂具有抗乌头碱致心律失常作用,且中药中、高剂量组作用显著。
2.中药低、中、高剂量组均可以降低氯化钙致PVBs发生率,中药中、高剂量组可以降低VF发生率,但无统计学差异(P>0.05)。与空白对照组比较,中药低、中、高剂量组均可显著延迟CA出现时间(P<0.01),并且可以明显增加CA出现时氯化钙用量(P<0.05,P<0.01,P<0.01);中药中、高剂量组还可显著延迟心律失常出现时间(P<0.01),且可显著增加心律失常出现时氯化钙用量(P<0.01)。中药不同剂量组间比较,与中药低剂量组比较,中药中、高剂量组可以显著延迟心律失常出现时间(P<0.01),并能够显著增加心律失常出现时氯化钙用量(P<0.01)；且中药高剂量组可以增加CA出现时氯化钙用量(P<0.05)。说明益气复脉合剂具有抗氯化钙致心律失常作用,且中药中、高剂量组作用显著。
3.空白对照组与中药组在大鼠体重、心率、收缩压、舒张压及平均动脉压方面无显著性差异(P>0.05),两组具有可比性。心电遥测1小时,中药组SPR和VTR低于空白对照组,但无统计学差异(P>0.05)；中药组SP个数显著低于空白对照组(P<0.05)。心电遥测2小时,中药组SP个数、PP对数及VT次数均显著低于空白对照组(P<0.05)。中药组与空白组在SP出现时间上无显著差异(P>0.05),而中药组较空白对照组可显著延长PP及VT时间(P<0.05)。说明中药益气复脉合剂具有抗异丙肾诱发心律失常作用,且长时间作用更显著。
4.中药组静息电位(RP)、超射(OS)、动作电位幅度(APA)、最大上升速率(Vmax)与空白对照组比较,Iso灌流前后均无显著差异(P>0.05)。Iso灌流前,中药组APD、APD50> APD90较空白对照组明显延长(P<0.05)；Iso灌流后,空白对照组与中药组APD较Iso灌流前明显延长(P<0.01,P<0.05),且空白对照组APD50、 APD90较Iso灌流前亦显著延长(P<0.01)；Iso灌流后,中药组APD、APD50、 APD90较空白对照组显著缩短(P<0.01),说明中药益气复脉合剂有对抗Iso引起APD延长的作用,可能与抑制平台期Ca2+电流和复极后期K+电流有关。
结论
1.益气复脉合剂具有抗乌头碱和氯化钙致室性心律失常作用,提示在生理状态下,益气复脉合剂具有抗室性期前收缩作用,且临床常用剂量(即中剂量)即可作用显著。
2.益气复脉合剂具有抗异丙肾致室性心律失常作用,提示在病理状态下,益气复脉合剂具有抗室性期前收缩作用,且较长时间作用更显著。
3.益气复脉合剂具有对抗异丙肾致APD延长的作用,其作用机制可能与抑制平台期Ca2+电流和复极后期K+电流有关。
The pathogenesis of premature ventricular beats(PVBs) is that ventricular with unusual self-discipline because of pathological changes, and when self-discipline absolutely or relatively exceeds the sinus node, they will be issued ectopic impulse, instead of controlling the activities of the heart, thus, generated the PVBs. Antiarrhythmic drugs affect myocardial cell membrane ion channels, changing the ion flow, thereby changing the electrophysiological characteristics of myocardial cells, and inhibiting the self-discipline of ectopic pacemaker, terminating of reentry, inhibiting depolarization and triggered excitement, thus play a role in the antiarrhythmic effect. While western antiarrhythmic drugs are almost exist potential arrhythmogenic effect. So there are some limitations in the treatment.
Chinese medicine shows certain advantages in the treatment of PVBs. Previously literatures report that single herb has different mechanisms of antiarrhythmic. The clinical palpitations patients are more with deficiency mixed syndromes. Its pathogenesis is mostly Qi deficiency and blood stasis, phlegm and blood stasis. Yiqifumai mixture has effect of replenishing Qi and vivid the blood, dispelling phlegm and calm senses, and has effective clinical applications. Therefore, the study is intended to evaluate the overall efficacy of antiarrhythmic of Yiqifumai mixture, and explain the mechanism of the anti-arrhythmic, in order to provide more complete and reliable support for the clinical treatment.
Purpose
It uses the classic models of aconitine, calcium chloride and isoproterenol to cause arrhythmias, and the small animals ECG telemetry technology, to evaluate the overall efficacy of Yiqifumai mixture on PVBs. It uses the patch-clamp technique, recording the impact of the action potential on cardiac myocytes. Furthermore, it describes the mechanisms of antiarrhythmic effect, in order to provide more complete and reliable support for the clinical treatment.
Method
Using aconitine, calcium chloride arrhythmogenic models and the SD rats are randomly divided into wihte type group (WT), Fulvtongmai mixture (low, medium, high dose) groups (LOW, MID, HIGH). Pumping the aconitine solution or calcium choride solution from the femoral vein in a constant speed, and record the time when PVBs, ventricular tachycardia (VT), ventricular fibrillation (VF) and cardiac arrest (CA) and arrhythmia appear. Calculating the incidence of PVBs, VT, VF and the dosage of aconitine and calcium chloride. Using isoprenaiine (Iso)-induced arrhythmia model on spontaneously hypertensive rats (SHR), and using ECG telemetry, recording whether there has single PVBs (SP), paired PVBs (PP), VT in WT group and Chinese Medicine group (CM), and statistic on the incidence of SPR, PP, VT and the numbers and the time of occurrence. They all use to evaluate the antiarrhythmic effects of Yiqifumai mixture. Using the collagenase method in acutely isolated rat left ventricular myocytes, and using patch clamp techique, to record the action potential of ventricular myocytes, in order to explore the antiarrhythmic mechanism of Yiqifumai mixture.
Result
1. Compared with the WT group, Every dose of CM groups can significantly delay the aconitine induced PVBs, VT and VF time (P<0.05, P<0.01, P<0.01), and significantly increased the aconitine dosage when VT appears(P<0.05, P<0.01, P<0.01); the MID and the HIGH groups also can significantly delay CA time (P<0.01), and significantly increase the dose of aconitine when PVBs, VT, VF and CA appear (P<0.01). Compared with the LOW group, the MID and the HIGH groups can significantly delay PVBs, VT and VF time (P<0.01), and can significanly delay CA time (P<0.05, P<0.01), and significantly increase the dose of aconitine when PVBs, VT, VF and CA appear (P<0.01). It suggests that Yiqifumai mixture has anti-arrhythmogenic effect of aconitine and the effect of the MID and the HIGH dose is much better.
2. Every dose of CM groups can reduce the incidence of PVBs, induced by Calcium chloride; the MID and the HIGH groups can reduce the incidence of VF, but there are no significant differences (P>0.05). Compared with the WT group, every dose of CM groups can delay CA time (P<0.01), and can increase the dose of Calcium chloride when CA appears (P<0.05, P<0.01, P<0.01); the MID and the HIGH groups also can significantly delay arrhythmia time (P<0.01), and can significantly increase the dose cf Calcium chloride when arrhythmia appears (P<0.01). Compared with the LOW group, the MID and the HIGH groups can significantly delay arrhythmia time (P<0.01), and can significantly increase the dose of Calcium chloride when arrhythmia appears (P<0.01), and the HIGH group can increase the dose of Calcium chloride when CA appears (P<0.05). It suggests that Yiqifumai mixture has anti-arrhythmogenic effect of calcium chloride and the effect of the MID and the HIGH dose is much better..
3. The WT group and the CM group have no significant difference in the body weight of rats, heart rate, systolic blood pressure, diastolic blood pressure and mean arterial pressure (P>0.05), the two groups were comparable. After1hour of ECG telemetry, the CM group is lower than the WT group in incidence of SP and VT, but there is no significant difference (P>0.05); the CM group is significantly lower than the WT group in the amount of SP (P<0.05). After2hours of ECG telemetry, the CM group is significantly lower than the WT group in the amount of SP, PP and VT (P<0.05); there has no significant difference in SP time (P>0.05), but the CM group can significantly increase the time of PP and VT (P<0.05). It suggests that Yiqifumai mixture has anti-arrhythmogenic effect of isoprenaline, and the longer, the more significant.
4. Compared with the WT group, the CM group has no significant difference in resting potential (RP), overshoot (OS), action potential amplitude (APA) and the maximum rate of rise (Vmax) whether Iso perfusion or not (P>0.05). Before Iso perfusion, compared with the WT group, the CM group can significantly extend APD, APD50and APD90(P<0.05). After Iso perfusion, the WT group and the CM group can significantly extend APD (P<0.01, P<0.05), and the WT group also can significantly extend APD50and APD90(P<0.01). After Iso perfusion, compared with the WT group, the CM group can significantly shortening APD, APD50and APD90(P<0.01). It shows that Yiqifumai mixture can against the prolongation of APD caused by Iso, maybe related to the inhibiton of the late plateau Ca2+current and repolarization K+current.
Conclusion
1. Yiqifumai mixture has anit-ventricular arrhythmogenic effect of aconitine and calcium chloride. It suggests that Yiqifumai mixture has effect of anit-premature ventricular beats in physiological conditions and it has significant effect in clinical dose (as the dose of the MID group).
2. Yiqifumai mixture has effects of anti-ventricular arrhythmogenic effect of isoproterenol. It suggests that Yiqifumai mixture has effect of anti-premature ventricular beats in pathological conditions, and the longer, the more significant.
3. Yiqifumai mixture can against the prolongation of APD caused by Iso. It's mechanism maybe related to the inhibiton of the late plateau Ca2+current and repolarization K+current.
中医药在室性期前收缩的治疗上显示了一定优势,既往文献报道单味中药存在不同的抗心律失常机制。临床上心悸患者多为虚实夹杂证,其病机多为气虚血瘀,痰瘀互阻,益气复脉合剂(原复律通脉合剂)具有益气活血,祛痰安神功效,且临床应用有效。因此,本研究意在评价益气复脉合剂抗室性期前收缩整体疗效,阐述其抗心律失常作用机制,为临床治疗提供更加完整、可靠的数据支持。
目的
采用乌头碱、氯化钙及异丙肾上腺素致心律失常经典模型的方法,利用小动物心电遥测技术,评价益气复脉合剂对室性期前收缩作用的在体疗效；利用膜片钳技术,记录益气复脉合剂对心肌细胞动作电位的影响,进一步阐述其抗心律失常作用机制,为临床治疗提供更加完整、可靠的数据支持。
方法
采用乌头碱、氯化钙致心律失常模型,随机分为空白对照组、益气复脉合剂(低、中、高剂量)组。由股静脉恒速泵入乌头碱溶液或氯化钙溶液,记录室性期前收缩(PVBs)、室性心动过速(VT)、室颤(VF)及心脏停搏(CA)和心律失常(Arrhythmia)出现时间,计算室性期前收缩(PVBs).室性心动过速(VT)、室颤(VF)的发生率及乌头碱、氯化钙用量。采用异丙肾诱发SHR大鼠心律失常模型,利用心电遥测技术,对空白对照组和中药组动物记录是否出现单发室性期前收缩(Single PVBs, SP),成对室性期前收缩(Paired PVBs, PP),室性心动过速(VT),并统计其发生率(SPR. PPR.VTR)、出现个数及出现时间。综合评价益气复脉合剂的抗心律失常作用。采用胶原酶法急性分离大鼠左心室肌细胞,利用膜片钳技术,记录心室肌细胞动作电位相关指标,探讨益气复脉合剂抗心律失常机制。
结果
1.与空白对照组比较,中药低、中、高剂量组可明显延迟乌头碱致PVBs、 VT及VF出现时间(P<0.05,P<0.01,P<0.01),并明显增加VT出现时乌头碱用量(P<0.05,P<0.01,P<0.01)；中药中、高剂量组还可显著延迟乌头碱致CA出现时间(P<0.01),并明显增加PVBs、 VF及CA出现时乌头碱用量(P<0.01)。中药不同剂量组间比较,与中药低剂量组比较,中药中、高剂量组可显著延迟PVBs.VT及VF出现时间(P<0.01),且能明显延迟CA出现时间(P<0.05,P<0.01),并可显著增加PVBS、 VT, VF及CA出现时乌头碱用量(P<0.01)。说明益气复脉合剂具有抗乌头碱致心律失常作用,且中药中、高剂量组作用显著。
2.中药低、中、高剂量组均可以降低氯化钙致PVBs发生率,中药中、高剂量组可以降低VF发生率,但无统计学差异(P>0.05)。与空白对照组比较,中药低、中、高剂量组均可显著延迟CA出现时间(P<0.01),并且可以明显增加CA出现时氯化钙用量(P<0.05,P<0.01,P<0.01);中药中、高剂量组还可显著延迟心律失常出现时间(P<0.01),且可显著增加心律失常出现时氯化钙用量(P<0.01)。中药不同剂量组间比较,与中药低剂量组比较,中药中、高剂量组可以显著延迟心律失常出现时间(P<0.01),并能够显著增加心律失常出现时氯化钙用量(P<0.01)；且中药高剂量组可以增加CA出现时氯化钙用量(P<0.05)。说明益气复脉合剂具有抗氯化钙致心律失常作用,且中药中、高剂量组作用显著。
3.空白对照组与中药组在大鼠体重、心率、收缩压、舒张压及平均动脉压方面无显著性差异(P>0.05),两组具有可比性。心电遥测1小时,中药组SPR和VTR低于空白对照组,但无统计学差异(P>0.05)；中药组SP个数显著低于空白对照组(P<0.05)。心电遥测2小时,中药组SP个数、PP对数及VT次数均显著低于空白对照组(P<0.05)。中药组与空白组在SP出现时间上无显著差异(P>0.05),而中药组较空白对照组可显著延长PP及VT时间(P<0.05)。说明中药益气复脉合剂具有抗异丙肾诱发心律失常作用,且长时间作用更显著。
4.中药组静息电位(RP)、超射(OS)、动作电位幅度(APA)、最大上升速率(Vmax)与空白对照组比较,Iso灌流前后均无显著差异(P>0.05)。Iso灌流前,中药组APD、APD50> APD90较空白对照组明显延长(P<0.05)；Iso灌流后,空白对照组与中药组APD较Iso灌流前明显延长(P<0.01,P<0.05),且空白对照组APD50、 APD90较Iso灌流前亦显著延长(P<0.01)；Iso灌流后,中药组APD、APD50、 APD90较空白对照组显著缩短(P<0.01),说明中药益气复脉合剂有对抗Iso引起APD延长的作用,可能与抑制平台期Ca2+电流和复极后期K+电流有关。
结论
1.益气复脉合剂具有抗乌头碱和氯化钙致室性心律失常作用,提示在生理状态下,益气复脉合剂具有抗室性期前收缩作用,且临床常用剂量(即中剂量)即可作用显著。
2.益气复脉合剂具有抗异丙肾致室性心律失常作用,提示在病理状态下,益气复脉合剂具有抗室性期前收缩作用,且较长时间作用更显著。
3.益气复脉合剂具有对抗异丙肾致APD延长的作用,其作用机制可能与抑制平台期Ca2+电流和复极后期K+电流有关。
The pathogenesis of premature ventricular beats(PVBs) is that ventricular with unusual self-discipline because of pathological changes, and when self-discipline absolutely or relatively exceeds the sinus node, they will be issued ectopic impulse, instead of controlling the activities of the heart, thus, generated the PVBs. Antiarrhythmic drugs affect myocardial cell membrane ion channels, changing the ion flow, thereby changing the electrophysiological characteristics of myocardial cells, and inhibiting the self-discipline of ectopic pacemaker, terminating of reentry, inhibiting depolarization and triggered excitement, thus play a role in the antiarrhythmic effect. While western antiarrhythmic drugs are almost exist potential arrhythmogenic effect. So there are some limitations in the treatment.
Chinese medicine shows certain advantages in the treatment of PVBs. Previously literatures report that single herb has different mechanisms of antiarrhythmic. The clinical palpitations patients are more with deficiency mixed syndromes. Its pathogenesis is mostly Qi deficiency and blood stasis, phlegm and blood stasis. Yiqifumai mixture has effect of replenishing Qi and vivid the blood, dispelling phlegm and calm senses, and has effective clinical applications. Therefore, the study is intended to evaluate the overall efficacy of antiarrhythmic of Yiqifumai mixture, and explain the mechanism of the anti-arrhythmic, in order to provide more complete and reliable support for the clinical treatment.
Purpose
It uses the classic models of aconitine, calcium chloride and isoproterenol to cause arrhythmias, and the small animals ECG telemetry technology, to evaluate the overall efficacy of Yiqifumai mixture on PVBs. It uses the patch-clamp technique, recording the impact of the action potential on cardiac myocytes. Furthermore, it describes the mechanisms of antiarrhythmic effect, in order to provide more complete and reliable support for the clinical treatment.
Method
Using aconitine, calcium chloride arrhythmogenic models and the SD rats are randomly divided into wihte type group (WT), Fulvtongmai mixture (low, medium, high dose) groups (LOW, MID, HIGH). Pumping the aconitine solution or calcium choride solution from the femoral vein in a constant speed, and record the time when PVBs, ventricular tachycardia (VT), ventricular fibrillation (VF) and cardiac arrest (CA) and arrhythmia appear. Calculating the incidence of PVBs, VT, VF and the dosage of aconitine and calcium chloride. Using isoprenaiine (Iso)-induced arrhythmia model on spontaneously hypertensive rats (SHR), and using ECG telemetry, recording whether there has single PVBs (SP), paired PVBs (PP), VT in WT group and Chinese Medicine group (CM), and statistic on the incidence of SPR, PP, VT and the numbers and the time of occurrence. They all use to evaluate the antiarrhythmic effects of Yiqifumai mixture. Using the collagenase method in acutely isolated rat left ventricular myocytes, and using patch clamp techique, to record the action potential of ventricular myocytes, in order to explore the antiarrhythmic mechanism of Yiqifumai mixture.
Result
1. Compared with the WT group, Every dose of CM groups can significantly delay the aconitine induced PVBs, VT and VF time (P<0.05, P<0.01, P<0.01), and significantly increased the aconitine dosage when VT appears(P<0.05, P<0.01, P<0.01); the MID and the HIGH groups also can significantly delay CA time (P<0.01), and significantly increase the dose of aconitine when PVBs, VT, VF and CA appear (P<0.01). Compared with the LOW group, the MID and the HIGH groups can significantly delay PVBs, VT and VF time (P<0.01), and can significanly delay CA time (P<0.05, P<0.01), and significantly increase the dose of aconitine when PVBs, VT, VF and CA appear (P<0.01). It suggests that Yiqifumai mixture has anti-arrhythmogenic effect of aconitine and the effect of the MID and the HIGH dose is much better.
2. Every dose of CM groups can reduce the incidence of PVBs, induced by Calcium chloride; the MID and the HIGH groups can reduce the incidence of VF, but there are no significant differences (P>0.05). Compared with the WT group, every dose of CM groups can delay CA time (P<0.01), and can increase the dose of Calcium chloride when CA appears (P<0.05, P<0.01, P<0.01); the MID and the HIGH groups also can significantly delay arrhythmia time (P<0.01), and can significantly increase the dose cf Calcium chloride when arrhythmia appears (P<0.01). Compared with the LOW group, the MID and the HIGH groups can significantly delay arrhythmia time (P<0.01), and can significantly increase the dose of Calcium chloride when arrhythmia appears (P<0.01), and the HIGH group can increase the dose of Calcium chloride when CA appears (P<0.05). It suggests that Yiqifumai mixture has anti-arrhythmogenic effect of calcium chloride and the effect of the MID and the HIGH dose is much better..
3. The WT group and the CM group have no significant difference in the body weight of rats, heart rate, systolic blood pressure, diastolic blood pressure and mean arterial pressure (P>0.05), the two groups were comparable. After1hour of ECG telemetry, the CM group is lower than the WT group in incidence of SP and VT, but there is no significant difference (P>0.05); the CM group is significantly lower than the WT group in the amount of SP (P<0.05). After2hours of ECG telemetry, the CM group is significantly lower than the WT group in the amount of SP, PP and VT (P<0.05); there has no significant difference in SP time (P>0.05), but the CM group can significantly increase the time of PP and VT (P<0.05). It suggests that Yiqifumai mixture has anti-arrhythmogenic effect of isoprenaline, and the longer, the more significant.
4. Compared with the WT group, the CM group has no significant difference in resting potential (RP), overshoot (OS), action potential amplitude (APA) and the maximum rate of rise (Vmax) whether Iso perfusion or not (P>0.05). Before Iso perfusion, compared with the WT group, the CM group can significantly extend APD, APD50and APD90(P<0.05). After Iso perfusion, the WT group and the CM group can significantly extend APD (P<0.01, P<0.05), and the WT group also can significantly extend APD50and APD90(P<0.01). After Iso perfusion, compared with the WT group, the CM group can significantly shortening APD, APD50and APD90(P<0.01). It shows that Yiqifumai mixture can against the prolongation of APD caused by Iso, maybe related to the inhibiton of the late plateau Ca2+current and repolarization K+current.
Conclusion
1. Yiqifumai mixture has anit-ventricular arrhythmogenic effect of aconitine and calcium chloride. It suggests that Yiqifumai mixture has effect of anit-premature ventricular beats in physiological conditions and it has significant effect in clinical dose (as the dose of the MID group).
2. Yiqifumai mixture has effects of anti-ventricular arrhythmogenic effect of isoproterenol. It suggests that Yiqifumai mixture has effect of anti-premature ventricular beats in pathological conditions, and the longer, the more significant.
3. Yiqifumai mixture can against the prolongation of APD caused by Iso. It's mechanism maybe related to the inhibiton of the late plateau Ca2+current and repolarization K+current.
引文
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