地尔硫卓对心房有效不应期和单相动作电位重构的干预研究

为研究地尔硫卓对快速心房起搏诱发的心房肌急性电重构的影响 ,将 4 0例无器质性心脏病的室上性心动过速患者射频消融成功后 30min随机分为两组 ,地尔硫卓组 15例 ,对照组 2 5例 ;地尔硫卓组给予药物干预 ,对照组以生理盐水替代 ,应用双极记录及单相动作电位记录法检测基础状态下、药物负荷量后 (即快速心房起搏前 )及4 0 0ms周长心房起搏后右心耳、高位右房、低位右房和His束周围等部位有效不应期 (ERP)和右房单相动作电位复极 90 %的时程 (MAPD90 )。结果 :对照组快速心房起搏后心房各部位ERP和右房MAPD90 较刺激前有明显缩短 ,地尔硫卓组心房快速起搏前后各部位ERP和右房MAPD90 无明显改变。结论 :快速心房起搏可使无器质性心脏病和心房颤动病史的患者心房ERP和MAPD90 明显缩短 ,地尔硫卓可阻止快速心房起搏诱发的心房ERP和MAPD90 的缩短 ,提示细胞内钙超载可能是心房ERP和单相动作电位重构的重要原因之一。     

扩张型心肌病兔电重构机制的初步探讨

目的:探讨扩张型心肌病(DCM)兔电重构的表现及机制。方法:耳缘静脉注射阿霉素建立DCM模型,采用接触电极记录心内膜单相动作电位(MAP)技术了解DCM时MAP各参数、心室有效不应期(ERP)和后除极电位的情况。结果:实验组MAP复极完成50%的时间(MAPD50),复极完成90%的时间(MAPD90)和ERP较对照组延长,MAPD50分别为(113.40±19.05)∶(80.83±11.69)ms,MAPD90分别为(174.10±25.69)∶(127.14±14.32)ms,ERP分别为(107.60±10.92)∶(88.33±9.37)ms,均差异有统计学意义(均P<0.05),并有3例动物出现后除极电位且1例诱发室性心动过速。结论:MAP复极时间和ERP的延长以及后除极电位的出现是DCM时电重构的主要表现,也可能是DCM发生室性心律失常的部分原因。     

四氢巴马汀对家犬心室肌单相动作电位时程使用依赖性的研究

目的 :利用单相动作电位 ( MAP)技术研究在整体条件下四氢巴马汀对家犬心室肌 MAP时程的使用依赖性。方法 :同时记录家犬 ( 12只 )右室心尖部的 MAP和体表标准 II导联心电图 ,比较给药前后和在窦性心律以及 2 3 0、2 60、2 90、3 2 0次 /min起搏频率下心室肌有效不应期 ( ERP)、MAP复极 5 0 % ( MAPD50 )和复极 90 %( MAPD90 )的变化。结果 :给药 3 0 min( 2 0 m g/kg)后 ,在同一起搏频率下 ,ERP、MAPD50 、和 MAPD90 均明显延长 ,与给药前相比差异有极显著性意义 ( P <0 .0 1) ;随起搏频率增加 ,ERP、MAPD50 和 MAPD90 逐渐缩短 ,但比较给药后不同起搏频率与窦性心律时的 ERP、MAPD50 和 MAPD90 变化率以及 ERP/MAPD90 比值的变化 ,则差异无显著性意义 ( P >0 .0 5 )。结论 :在整体条件下 ,四氢巴马汀无逆向使用依赖性。     

大鼠左心房肌单相动作电位的增龄性变化

目的　研究年龄对大鼠左心房肌单相动作电位(monophasicactionpotential,MAP)的影响。方法　选取实验用Wistar大鼠4 0只,按出生年龄分为青年组、成年组、中年组及老年组,每组10只。体外Langendorff灌流心脏,右心室刺激。分别记录各组左心房肌在4 0 0ms刺激周长下动作电位复极到90 %、5 0 %及2 0 %时的单相动作电位时程(MAPD90 )、MAPD50 、MAPD2 0 和心房有效不应期,以及在不同刺激周长下的MAPD90 、MAPD50 、MAPD2 0 。结果　MAPD各时相和有效不应期都随着年龄的增加而出现延长(P <0 .0 1) ;但老年组缩短。在同一年龄组中,刺激频率增加使动作电位时程都相应缩短,以MAPD90 明显;中年组MAPD改变明显。结论　年龄是影响心脏电活动重要的独立因素之一。     

年龄对大鼠左室心肌单相动作电位的影响

目的研究年龄对大鼠心室肌单相动作电位(monophasic action potential, MAP)影响.方法按月龄选取Wistar大鼠,分为青龄组和老龄组.体外Langendorff灌流心脏,右心室予以刺激,左心室心外膜记录单相动作电位.分别记录两组在相同刺激周长(400 ms)下动作电位,分析其复极到90%、50%及20%的时程(MAPD90、MAPD50、MAPD20),以及两组在不同刺激周长下MAP及时程. 结果在相同刺激周长下,老龄组大鼠心室肌MAP各时相均明显长于青龄组(P<0.01).刺激频率增加使大鼠心室肌MAPD缩短,老龄组大鼠动作电位时程MPAD90缩短较青龄组明显.结论年龄是影响心脏电活动的重要因素之一.     

大鼠心房肌电生理特性的增龄性变化

目的探讨年龄对心房肌单相动作电位(MAP)和有效不应期(ERP)的影响,及其与心房颤动(房颤)的关系。方法选取Wistar大鼠40只分为青年组、成年组、中年组和老年组4组。Langendorff体外灌流心脏。分别测量各组心房肌在400ms刺激周长下MAP复极到90%、50%及20%时的时程(MAPD90、MAPD50、MAPD20)和ERP,以及其他不同刺激周长下的MAPD。结果在400ms刺激周长下,4组大鼠右心房肌MAPD90随年龄增长而逐渐延长〔(75±5)(、123±8)(、140±11)和(140±14)ms,均为P<0.01〕;而左心房肌青年组至中年组延长分别为〔(60±4),(120±3),(139±7)〕,老年组缩短〔(102±14)ms,均为P<0.01〕。心房肌ERP的增龄性变化规律与MAPD90相同。刺激周长从400ms缩短到250ms,右心房肌MAPD90缩短程度从青年组到老年组逐渐增加;左心房肌以老年组缩短程度最小。结论左右心房肌电生理特性增龄性变化规律不同。老年期心房电生理变化可能有利于房颤的发生。     

阵发性心房颤动患者心房复极离散度的研究

目的　通过记录阵发性心房颤动 (房颤 )患者心房单相动作电位 (MAP) ,分析心房复极离散度与房颤发生的关系。方法　特发性阵发性房颤患者与无自发房颤病史的阵发性室上性心动过速患者各 1 5例 ,均接受心内电生理检查和 /或导管射频消融治疗。两根 MAP电极于右心房共取 4～ 1 0个不同部位进行同步的窦性心律基础刺激 (S1)及期前刺激 S2 时的 MAP记录。测量、计算心房复极离散度(RTd)及动作电位时限和局部冲动时间的离散度 (APDd、ATd)。　结果　窦性心律时房颤组最大 RTd显著大于对照组 (1 2 3 .69± 54.67) ms比 (64 .2 5± 2 3 .2 9) ms,(P<0 .0 1 )。其差异主要来源于 APDd(1 1 5.0 0± 4 6.90 ) ms比 (57.56± 3 3 .57) ms,(P<0 .0 1 ) ,ATd差异无显著性。随 S1、S2 的加入 ,各组局部激动时间和离散度逐渐增大 ,而动作电位时限逐渐缩短 ,且房颤组的这种改变程度显著大于对照组。在S1时无房颤发生 ,加入期前刺激时 ,大多数房颤组患者均多次诱发出短阵房颤。其诱发率及次数均显著高于对照组。　结论　研究结果表明 ,MAP记录技术是临床观察、分析心房复极离散度及其在阵发性房颤中的作用的较佳方法。心房复极离散度的增加是阵发性房颤发生的重要因素。期前刺激时动作电位时限的缩短和离散以及传导障碍在     

心房颤动中钙耦联蛋白表达的实验研究

采用逆转录聚合酶链式反应 (RT PCR)方法研究起搏房颤 (AF)模型心房肌钙耦联蛋白———L型钙通道α1c亚基和肌浆网Ca2 + ATP酶的基因表达情况以及药物的干预作用。选择成年杂种犬 15条 ,随机分为起搏组 (P组 )、起搏及口服维拉帕米组 (PV组 )和对照组 (C组 )。采用心房猝发刺激诱发AF。其中P组和PV组的犬在诱发AF后置入起搏脉冲发生器作心房快速 ( 4 0 0次 /分 )起搏 7天。PV组的犬于起搏第 2天起给予维拉帕米缓释剂 12 0mg/天口服。第 7天再次诱发AF后将动物处死 ,于左、右心房和房间隔部位取材进行RT PCR扩增。结果 :心房快速起搏 7天后 ,阵发性AF和持续性AF的发生率明显增加。而加用维拉帕米后AF的发生率和起搏前没有差异。以 β actin为内参照的RT -PCR结果显示起搏组心房肌的L型钙通道α1c亚基和肌浆网Ca2 + ATP酶的mRNA水平明显降低(和C组相比分别降低 4 3 %和 4 0 %,P <0 .0 1)。而PV组第 7天心房肌L型钙通道α1c亚基和Ca2 + ATP酶的mRNA水平和C组相比则没有显著差异 (P >0 .0 5 )。心房不同部位之间的mRNA水平没有差异。结论 :心房起搏AF模型中心房肌细胞钙耦联蛋白L型钙通道α1c亚基和肌浆网Ca2 + ATP酶的基因表达明显下调 ;钙通道阻断剂维拉帕米可预防心房电重构和心房肌钙耦联蛋白的下调。     

心房细胞的电重构与逆向电重构的研究

目的采用经典的玻璃微电极技术,观察快速起搏及自主神经递质、β受体阻滞剂和钙通道阻滞剂对心房肌细胞跨膜动作电位及其恢复过程的影响,探讨观察房性快速性心律失常中的电重构(ER)和逆向电重构(RER)现象。方法健康豚鼠35只取出心脏,剪下左心耳,取大约2×5mm大小的肌条。用充满3mol/L氧化钾的玻璃微电极插入心房肌,记录动作电位。观察复极30%、50%、90%时的动作电位时程(APD30、APD50、APD90)、有效不应期(ERP)、动作电位振幅(APA)、静息电位(RMP)。灌流台氏液中分别加入丙基肾上腺素(ISO)、乙酰胆碱(Ach)、去甲肾上腺素(NA),艾司洛尔(Esm)和地尔硫卓(Dil)平衡20min后记录上述指标并观察其恢复过程。结果快速心房刺激可出现明显的心房电重构,心房快速刺激终止后电重构特性逐步恢复,表现为逆向电重构。乙酰胆碱和丙基肾上腺素可延长快速起搏后动作电位和有效不应期的恢复。艾司洛尔和地尔硫卓均可改善短时间快速刺激后动作电位的恢复。我们提出的心脏电学顿抑是心脏的重要电生理特性之一。     

粉防己碱对家犬在体心脏单相动作电位的影响

目的:研究粉防己碱(Tet)对家犬在体心室肌单相动作电位(MAP)和有效不应期(ERP)的影响,探讨其抗心律失常的可能机制。方法:家犬14只,随机分为Tet组和维拉帕米(Ver)组,记录右室心内膜MAP及心电图Ⅱ导联,比较不同剂量的Tet和Ver对MAP振幅(MAPA)、复极化达50％和90％一点到MAP上升支的水平距离(MAPD50、MAPD90)、ERP及ERP/MAPD90。结果:Tet引起窦性心率减慢,随剂量增加(3～12 mg/kg)ERP延长、ERP/MAPD90增大,但对MAPA、MAPD50、MAPD90无明显影响;而Ver除延长ERP,增大ERP/MAPD90,还缩短MAPD50、MAPD90。结论:Tet对MAP的影响可能除钙拮抗作用外,还有别的离子基础;延长ERP、增大ERP/MAPD90可能是其抗心律失常的机制。     

Atrial fibrillation in the goat induces changes in monophasic action potential and mRNA expression of ion channels involved in repolarization

INTRODUCTION: Sustained atrial fibrillation (AF) is characterized by a marked shortening of the atrial effective refractory period (AERP) and a decrease or reversal of its physiologic adaptation to heart rate. The aim of the present study was to investigate whether the AF-induced changes in AERP in the goat are associated with changes in the atrial monophasic action potential (MAP) and whether an abnormal expression of specific ion channels underlies such changes. METHODS AND RESULTS: Following thoracotomy, MAPs were recorded from the free wall of the right atrium both before induction of AF (control) and after cardioversion of sustained AF (>2 months) in chronically instrumented goats. In control goats, MAP duration at 80% repolarization (MAPD80) shortened (P < 0.01) from 132+/-4 msec during slow pacing (400-msec interval) to 86+/-10 msec during fast pacing (180 msec). After cardioversion of sustained AF, the MAPD80 during slow pacing was as short as 67+/-5 msec (electrical remodeling). Increasing the pacing rate resulted in prolongation (P = 0.02) of the MAPD80 to 91+/-6 msec. Also, MAPD20 (20% repolarization) shortened (P = 0.05) from 32+/-4 msec (400 msec) to 14+/-7 msec (180 msec) in the control goats, whereas it prolonged (P = 0.03) from 20+/-3 msec (400 msec) to 33+/-5 msec (180 msec) in sustained AF. mRNA expression of the L-type Ca2+ channel alpha1c gene and Kv1.5 potassium channel gene, which underlie ICa and IKur, respectively, was reduced in sustained AF compared with sinus rhythm by 32% (P = 0.01) and 45% (P < 0.01), respectively. No significant changes were found in the mRNA levels of the rapid Na+ channel, the Na+/Ca2+ exchanger, or the Kv4.2/4.3 channels responsible for Ito. CONCLUSION: AF-induced electrical remodeling in the goat comprises shortening of MAPD and reversal of its physiologic rate adaptation. Changes in the time course of repolarization of the action potential are associated with changes in mRNA expression of the alpha subunit genes of the L-type Ca2+ channel and the Kv1.5 potassium channel.     

Sotalol reverses remodeled action potential in patients with chronic atrial fibrillation but does not prevent arrhythmia recurrence

INTRODUCTION: Recurrence of atrial fibrillation (AF) may be related to AF-induced electrical remodeling characterized by shortening of the atrial action potential duration (APD) and loss of its rate adaptation. We investigated the effects of pretreatment with oral d,l-sotalol on rate-dependent changes in atrial monophasic action potential (MAP) duration after cardioversion of chronic AF with reference to the efficacy in preventing the arrhythmia recurrence. METHODS AND RESULTS: MAPs were recorded from the right atrium at six pacing cycle lengths (CLs) from 300 to 750 ms in 19 chronic AF patients after electrical cardioversion; 9 had been pretreated with oral d,l-sotalol (196 +/- 42 mg/day) for 7 days and 10 were untreated. MAP duration at 90% repolarization (MAPD90) in 11 control patients increased progressively with increases in CLs from 209 +/- 19 ms at CL = 300 ms to 264 +/- 28 ms at CL = 750 ms. In AF patients without sotalol, the CL-MAPD relation was shifted downward and flattened at longer CLs; MAPD90 values were 206 +/- 11 ms and 227 +/- 16 ms at CLs of 300 and 750 ms, respectively. MAPD90 values at CLs > or =500 ms in AF were significantly shorter than controls. In AF patients with sotalol, the normal CL-MAPD relation was preserved; MAPD90 increased from 226 +/- 19 ms to 282 +/- 46 ms in the CL range. AF recurred within 2 weeks after cardioversion in 14 of 24 patients pretreated with d,l-sotalol (216 +/- 51 mg/day) despite of continuation of sotalol treatment. CONCLUSION: Sotalol reverses AF-induced decrease in MAPD adaptation to rate in the atria of chronic AF patients, but this effect does not lead to prevention of AF recurrence.     

心房颤动24h和48h对犬心房肌有效不应期及L型钙电流的影响

目的 研究犬心房颤动（房颤）持续24h和48 h,心房肌有效不应期和L型钙电流变化的一致性及其机制.方法 健康成年杂种犬18只,分为对照组、24 h房颤组、48 h房颤组,每组6只.600次/min起搏高右心房建立犬房颤模型,应用程序刺激的方法测定右心房有效不应期（ERP）,通过Langendorff左回旋支灌流分离心房肌细胞,并通过全细胞膜片钳技术记录L型钙电流（ICa-L）变化.应用免疫组织化学方法检测各组心房组织L型电压依赖性钙通道（LVDCC）α1c蛋白表达.用图像分析系统对组织化学抗原表达进行半定量分析.结果 所有实验动物均可诱发出房颤.心房ERP的变化在最初6h较对照组明显缩短,后直至48 h呈进行性缩短.快速起搏6h后ERP（129.50±8.64）ms较对照组（141.00±15.23）ms缩短（12.13±2.24）ms（P＜0.01）,24 h后心房ERP（123.00± 13.37） ms缩短（19.23±2.14）ms（P＜0.01）,48 h缩短（28.15±4.26）ms（P＜0.01）.同时在房颤持续过程中24h房颤可引起ICa-L电流密度（-4.83±0.30）pA/pF较对照组（-6.69±0.08）pA/pF减小,48 h（-3.70±0.50）pA/pF减少的程度更重.24 h房颤及48 h房颤犬的左、右心房组织LVDCC α1c蛋白表达均较对照组明显减少（P＜0.05）,48 h房颤组减少程度更重（P＜0.01）.结论 房颤持续24 h,心房肌ERP显著缩短、ICa-L密度降低.房颤持续48 h仍然维持L型钙通道改变特征.提示：钙通道阻断剂可用于持续24 h房颤,预防房颤复发.     

维拉帕米对快速心房起搏家兔心房有效不应期和单相动作电位的影响

目的研究维拉帕米对快速心房起搏家兔心房有效不应期(AERP)和单相动作电位(MAP)的影响,探讨其抗心律失常的机制。方法 24只家兔分为对照组、快速起搏组和维拉帕米组,每组各8只。经颈内静脉将电极置入右心房。分别测定各组基础状态,以600次/min行快速心房起搏和快速起搏同时给予药物维拉帕米后测定2、4、6、8 h的心房有效不应期(AERP_(200)和AERP_(150))和MAP_(90)。结果快速心房起搏组在不同基础刺激周长作用下的AERP缩短,AERP_(200-150)的频率适应性不良,P_8与起搏前P_0比较差异有统计学意义(P<0.05),同时MAP_(90)相应缩短。维拉帕米组AERP基本无改变,AERP_(200-150)频率适应性维持,MAP_(90)无明显改变(P>0.05)。结论维拉帕米可能因减轻钙超载而抑制快速心房起搏所致电重构,即同时延长AERP和MAP,发挥其抗心律失常作用。     

Prediction of terminal atrial myocardial repolarisation from incomplete phase 3 data

The duration of the monophasic action potential (MAP) carries prognostic antiarrhythmic information when the recording is done during sinus rhythm (SR) after DC conversion of atrial fibrillation (AF). This study analyses whether it is possible to predict MAP duration during sinus rhythm by analysing the atrial MAP during AF, even though complete myocardial repolarisation is never reached during this arrhythmia. We have therefore evaluated the estimated duration of the action potential (AP) and MAP by exponential extrapolation of phase 3 data. (1) AP studies were done on 11 human atrial myocardial specimens. Resting membrane potential (RMP) and AP duration were better identified when more data obtained during repolarisation were used for prediction. Thus the predicted RMP deviated on average by -0.4% of AF amplitude from the real RMP level when data to 90% repolarisation were used for extrapolation. AP duration at 90% repolarisation correlated well with the real AP duration (r = 0.88) at this level of data aquisition. (2) Continuous recording of atrial MAPs was done in 15 patients during AF and in 12 of these during SR after DC conversion. Resting myocardial repolarisation level during AF, RP(EST), and estimated MAP duration, MAPD(EST), could be calculated by exponential extrapolation in 12 patients. The actual repolarisation during fibrillation reached below 90% of the RP(EST) level in eight patients and below 70% in all 12. The MAP duration during SR could be predicted with increasing precision when data closer to the RP(EST) were used for calculation of MAPD(EST). Thus MAPD(EST) correlated well with SR MAP duration when data reaching at least 90% of RP were used (r = 0.85).(ABSTRACT TRUNCATED AT 250 WORDS)     

Ionic mechanisms of electrical remodeling in human atrial fibrillation

OBJECTIVES: Atrial fibrillation (AF) is associated with a decrease in atrial ERP and ERP adaptation to rate as well as changes in atrial conduction velocity. The cellular changes in repolarization and the underlying ionic mechanisms in human AF are only poorly understood. METHODS: Action potentials (AP) and ionic currents were studied with the patch clamp technique in single atrial myocytes from patients in chronic AF and compared to those from patients in stable sinus rhythm (SR). RESULTS: The presence of AF was associated with a marked shortening of the AP duration and a decreased rate response of atrial repolarization. L-type calcium current (ICa,L) and the transient outward current (Ito) were both reduced about 70% in AF, whereas an increased steady-state outward current was detectable at test potentials between -30 and 0 mV. The inward rectifier potassium current (IKI) and the acetylcholine-activated potassium current (IKACh) were increased in AF at hyperpolarizing potentials. Voltage-dependent inactivation of the fast sodium current (INa) was shifted to more positive voltages in AF. CONCLUSIONS: AF in humans leads to important changes in atrial potassium and calcium currents that likely contribute to the decrease in APD and APD rate adaptation. These changes contribute to electrical remodeling in AF and are therefore important factors for the perpetuation of the arrhythmia.     

心房电重构与房颤关系的基础研究

目的检查观测心房电生理改变与房颤（AF）发生和持续的关系,探讨心房电重构与房颤的内在联系。方法健康成年杂种犬14只（雌雄不拘,体重10．0～12．5kg）,随机分为2组：对照组（A组）和起搏组（B组）。右侧开胸将电极置于右心房,以400次／min的频率快速起搏右心房（A组只手术不起搏）,分别于实验开始及起搏6h后对每只犬进行电生理检查,测定心房有效不应期（AERP）。起搏开始及起搏后测定burst刺激诱发房颤的频率和持续时间。结果A组在整个时间内AERP无变化,B组心房快速起搏后,AERP明显缩短。A、B两组起搏前房颤的频率和持续时间差异无统计学意义。A组起搏前、后房颤的频率和持续时间无变化,B组心房快速起搏后房颤的频率增多,持续时间延长。结论快速心房起搏可以引起心房有效不应期缩短,即心房电重构。心房电重构造成的心房有效不应期等电生理变化促进了房颤的发生和维持,是心房电重构与房颤关系的基础。     

Electrical remodeling in fibrillating canine atrium: action potential alternans during rapid atrial pacing and late phase 3 early afterdepolarization after cessation of rapid atrial pacing

Sustained atrial fibrillation (AF) was induced by atrial burst pacing, and monophasic action potentials (MAPs) were recorded. MAP alternans was observed at a cycle length (CL) of 167.5 ± 28.2 msec before burst pacing and 201.3 ± 40.2 msec after burst pacing. AF > 5 minutes duration was induced in 1 dog in the control condition but in all 8 dogs after burst pacing. The difference in RA MAPD(80) of the first spontaneous beat and steady-state sinus rhythm was significantly larger after atrial burst pacing than before atrial burst pacing (31.5 ± 15.9 msec versus 8.2 ± 9.0 msec) In 4 dogs, late phase 3 early after depolarization was observed after rapid atrial pacing. Rapid atrial pacing-induced electrical remodeling includes APD alternans during rapid atrial pacing and also causes an increase in the MAPD of the initial several beats and the development of late phase 3 early afterdepolarizations after a sudden increase in CL.     

四氢巴马汀对家犬在体心脏单相动作电位和有效不应期影响的研究

利用单相动作电位 (MAP)技术 ,研究在整体条件下四氢巴马汀 (THP)对家犬在体心脏MAP和有效不应期(ERP)的影响 ,从而探讨THP在整体条件下的抗心律失常机制。家犬 8只 ,体重 12 .5± 3.0 ( 10～ 15 )kg。同时记录家犬右室心尖部的MAP和体表Ⅱ导联心电图 (ECG) ,比较在窦性心律下用药前和用药后 10 ,2 0 ,30min的ERP、MAP复极 5 0 %时程 (MAPD5 0 )和复极 90 %时程 (MAPD90 )以及MAP振幅 (MAPA)的变化。结果 :用药后 10min ,各参数均无明显变化 (P >0 .0 5 ) ;用药 2 0min后 ,ERP、MAPD5 0 和MAPD90 与用药前相比 ,均明显延长 (分别为 139± 18msvs 12 4±18ms,12 6± 16msvs112± 15ms ,16 4± 2 5msvs 140± 16ms,P均 <0 .0 1) ,但用药前后ERP MAPD90 的比值无显著性变化 (P >0 .0 5 )。结论 :THP通过延长动作电位 2相和 3相时程 ,使ERP和MAPD90 平行延长 ,但不改变用药前后ERP MAPD90 比值 ,从而具有增加心肌电稳定性的作用 ,推测此是其具有抗室性心律失常的作用的可能机制