Rate-dependent prolongation of action potential duration in isolated rat ventricular myocytes

Rate-dependent alterations of action potential duration (APD) in rat ventricular myocytes were investigated. Action potentials of the isolated myocytes were recorded with patch electrodes containing EGTA (11 mM), and showed a marked rate-dependent prolongation in the APD (0.2–5 Hz). This prolongation was significantly inhibited in the presence of 4-aminopyridine (4-AP), a blocker of the transient outward K⁺ current (I_to). Thus, the rate-dependent decrease in I_to may underlie the change in APD. In contrast, the action potentials recorded from rat ventricular papillary muscles with conventional microelectrodes did not show rate-dependent alterations in the APD, i.e., the APD remained practically unaltered at the frequency range of 0.2–5 Hz. These results suggest that the rate-dependent prolongation of APD (due to rate-dependent blockade of I_to) becomes evident when the intracellular Ca²⁺ was chelated by the internal application of EGTA via patch pipette. We speculate that the rate-dependent prolongation of APD (via decreases in I_to) is masked in the ventricular papillary muscles, probably due to rate-dependent decreases in the inward current (e.g., electrogenic Na⁺–Ca²⁺ exchange current) that is regulated by the intracellular calcium.     

Barium-induced spontaneous activity in sheep cardiac Purkinje fibers

We used intracellular microelectrodes to study the electrophysiological effects of low barium concentrations (1 ? 4 × 10 ⁵m) on sheep cardiac Purkinje fibers. The main effect of barium was an increase in action potential duration (APD) both at ?60 mV (APD_?60) and at 100% repolarization (APD₁₀₀). The prolongation of APD was greater at a lower (30/min) than at a higher driving rate (120/min). Barium significantly modified the normal linear relationship between driving rate and APD. The effects of barium on APD were enhanced by lowering [K⁺]₀ and antagonized by increasing [Ca²⁺]₀. Barium caused a slowing of phase 3 repolarization, a steepening of diastolic depolarization and induced spontaneous activity in the resting potential range during the interruption of the drive. The first spontaneous action potential was usually preceded by an oscillatory potential. By means of several procedures (lowering [K⁺]₀, increasing [Ca^2?]₀, increasing the driving rate) it was possible to identify two separate mechanisms underlying the initiation of spontaneous activity: (1) enhancement of normal diastolic depolarization and (2) induction of oscillatory afterpotentials. Finally, barium induced repetitive activity through early afterdepolarizations. We conclude that in Purkinje fibers low barium concentrations cause a lengthening of APD and can induce spontaneous activity by means of at least three different mechanisms. The main factor underlying the barium effects seems to be a reduction in potassium conductance.     

Species plays an important role in drug-induced prolongation of action potential duration and early afterdepolarizations in isolated Purkinje fibers

INTRODUCTION: Although isolated Purkinje fibers (PFs) often are used to evaluate the electrophysiologic effects of new drugs in terms of prolongation of action potential duration (APD) and induction of early afterdepolarizations (EADs), species differences in this respect remain elusive. We evaluated potential species-specific differences in drug-induced prolongation of APD and EADs in isolated PF from various species. METHODS AND RESULTS: Using a microelectrode technique, PFs (n = 7 to 11 per species) were isolated from hearts of rabbits, guinea pigs, dogs, swine, goats, or sheep, superperfused in Tyrode's solution with dofetilide (1 x 10(-8) M) or quinidine (1 x 10(-5) M) for 25 minutes, and stimulated at 1 Hz for 20 minutes and at 0.2 Hz for another 5 minutes. Dofetilide increased APD at 90% repolarization (APD90) at 1 Hz by 83% (rabbit), 24% (guinea pig), 65% (dogs), 18% (swine), 61% (goat), and 30% (sheep), and prolonged APD90 at 0.2 Hz by 187% (rabbit), 31% (guinea pig), 154% (dog), 17% (swine), 61% (goat), and 8% (sheep). Similarly, quinidine changed APD90 by 93% (rabbit), 0% (guinea pig), 16% (dog), -3% (swine), 0% (goat), and -24% (sheep) at 1 Hz, and by 124% (rabbit), 15% (guinea pig), 53% (dog), 17% (swine), 11% (goat), and -39% (sheep) at 0.2 Hz in PF. During superfusion of dofetilide or quinidine, EADs occurred in most preparations in rabbit PFs at 0.2 Hz, but not in any of the PFs from other species at 0.2 Hz. CONCLUSION: Our study demonstrates that species plays an important role in the response of PF to drug-induced prolongation of APD and EADs. Rabbit PFs constitute the most sensitive model for detecting drug-induced, potential long APD and proarrhythmogenic effects in vitro.     

替米沙坦对牵张刺激乳大鼠心房肌细胞短暂外向钾电流和动作电位的影响

目的探讨替米沙坦对牵张刺激乳大鼠心房肌细胞瞬时外向钾电流（Ito）和动作电位（AP）的影响。方法利用胰酶与Ⅱ型胶原酶混合酶解,并结合差速贴壁和5-溴脱氧尿嘧啶核苷处理得到纯化的乳大鼠心房肌细胞。实验分对照组、牵张组、替米沙坦（1μmol/L）组。采用全细胞膜片钳技术分别记录三组Ito和AP。结果在＋20~＋60 mV刺激电压水平,Ito电流密度（pA/pF）：牵张组低于对照组[＋20 mV和＋60 mV分别为（0.8±0.3）vs（2.1±0.8）和（1.6±0.4）vs（12.1±3.0）;P均〈0.01],替米沙坦组[＋20 mV和＋60 mV分别为（1.4±0.3）和（6.7±1.3）较牵张组增大,P均〈0.01]。牵张组AP复极50%、90%时程（APD50、APD90）较对照组明显缩短[（9.6±1.3 ms）vs（15.5±2.4）ms,（29.9±2.9）ms vs（56.3±3.6）ms,P均〈0.01,n=9],替米沙坦组[APD50、APD90分别为（11.7±2.0）和（41.4±4.6）ms]较牵张组APD延长（P均〈0.05）。结论牵张刺激可降低乳大鼠心房肌细胞Ito电流密度、缩短APD;替米沙坦干预可抑制牵张刺激的此作用。     

大鼠肥在左心室肌细胞瞬间外向性钾流的意义

目的 了解大鼠肥大左心室肌细胞瞬间外向性钾流（Ito)意义。方法 应用微电极技术记录动作电位、膜片钳全细胞记录技术记录Ito。观察比较自发性高血压大鼠与正常血压大鼠左心室肌细胞Ito。结果 与正常血压大鼠比较,高血压大鼠心脏重量、心脏重量／体重及平均细胞膜电容均非常显著增加（P＜0．01）,左心室肌细胞APD50及APD90非常显著延长（P＜0．01）,Ito密度非常显著降低（P＜0．01）,但Ito通道的门控动力学无差异。结论 自发性高血压大鼠Ito密度降低是导致动作民位时程延长的原因之一。     

Transient-outward K+ channel inhibition facilitates L-type Ca2+ current in heart

BACKGROUND: Transient outward current (I(to)) and L-type calcium current (I(Ca)) are important repolarization currents in cardiac myocytes. These two currents often undergo disease-related remodeling while other currents are spared, suggesting a functional coupling between them. Here, we investigated the effects of I(to) channel blockers, 4-aminopyridine (4-AP) and heteropodatoxin-2 (HpTx2), on I(Ca) in cardiac ventricular myocytes. METHODS AND RESULTS: I(Ca) was recorded in enzymatically dissociated mouse and guinea pig ventricular myocytes using the whole-cell voltage clamp method. In mouse ventricular myocytes, 4-AP (2 mM) significantly facilitated I(Ca) by increasing current amplitude and slowing inactivation. These effects were not voltage-dependent. Similar facilitating effects were seen when equimolar Ba2+ was substituted for external Ca2+, indicating that Ca2+ influx is not required. Measurements of Ca2+/calmodulin-dependent protein kinase (CaMKII) activity revealed significant increases in cells treated with 4-AP. Pretreatment of cells with 10 microM KN93, a specific inhibitor of CaMKII, abolished the effects of 4-AP on I(Ca.) To test the requirement of I(to), we studied guinea pig ventricular myocytes, which do not express I(to) channels. In these cells, 2 mM 4-AP had no effect on I(Ca) amplitude or kinetics. In both cell types, Ca2+-induced I(Ca) facilitation, a CaMKII-dependent process, was observed. However, 4-AP abolished Ca2+-induced I(Ca) facilitation exclusively in mouse ventricular myocytes. CONCLUSION: 4-AP, an I(to) blocker, facilitates L-type Ca2+ current through a mechanism involving the I(to) channel and CaMKII activation. These data indicate a functional association of I(Ca) and I(to) in cardiac myocytes.     

铬对绵羊浦肯野纤维起搏离子流(If)的影响

目的探索Cr3+对自律细胞起搏离子流If的影响.方法双微电极电压钳制术,观测Cr3+对起搏离子流If,在膜电位-70～120 mV各指令电位的If幅值和激活时间的改变.结果Cr3+对起搏离子流If有明显的抑制作用,If幅值降低(n=7,P＜0.05～0.01),激活曲线向超极化方向移位,激活时间无变化.结论Cr3+对起搏离子流If有抑制作用,从而使正常的自律活动有所减弱,即可能具有一定的抗心律失常作用.     

Regulation of transient outward current in human atrial myocytes by protein tyrosine kinase pathway

INTRODUCTION: Regulation of transient outward current (I(to)) in human myocytes is unclear. The present study investigated the effect of protein tyrosine kinase (PTK) inhibitors on I(to) in human atrial myocytes. METHODS AND RESULTS: Atrial myocytes were isolated enzymatically from biopsies of human right atrial appendage obtained from patients undergoing coronary artery bypass surgery. I(to) was recorded by the whole-cell patch-clamp technique in voltage-clamp configuration. Two groups of PTK inhibitors, the ATP binding site PTK inhibitors genistein and AG957 and the protein substrate PTK inhibitors ST638 and PP2, significantly inhibited I(to) in a concentration-dependent manner, with a potency order of genistein>AG957>ST638>PP2. At test pulse potential of +60 mV, I(to) was inhibited by 28% +/- 3%, 59% +/- 3%, and 89% +/- 3% by 15, 50, and 100 microM genistein, respectively. Daidzein and PP3, inactive analogues of genistein and PP2, respectively, did not produce any inhibitory effects on I(to). In addition to the inhibition of I(to) amplitude, the protein substrate PTK inhibitors ST638 and PP2 significantly accelerated I(to) inactivation (current decay) and delayed recovery from inactivation. Inhibition of protein tyrosine phosphatase partially reversed the effect of genistein. Stimulation or inhibition of serine/ threonine kinases (PKA, PKC, and PKG) did not change I(to) or alter the inhibitory response of PTK inhibitors on I(to). CONCLUSION: In human atrial cells, the PTK pathway plays an important role in the regulation of basal I(to), independent of serine/threonine kinases.     

胡椒碱对H2O2致兔心房肌细胞动作电位时程及L型钙电流异常的保护作用

目的:研究胡椒碱(PIP)对H2O2引起的单个兔心房肌细胞动作电位时程（APD）及L型钙电流(ICa,L)异常的保护作用。方法:采用全细胞膜片钳技术,观察10和50 μmol/L的H2O2引起单个兔心房肌细胞APD及ICa,L的改变,以及预先应用7 μmol/L的PIP对其的作用。结果:7 μmol/L的PIP对正常兔心房肌细胞APD、ICa,L及L型钙通道动力学无明显影响。在10和50 μmol/L的H2O2作用下,兔心房肌细胞APD50和APD90明显缩短(P<0.05),静息膜电位（RMP）绝对值显著下降(P<0.05),ICa,L峰值由(39.3±5.4) pA/pF降低至(32.8±2.0) pA/pF(P<0.05),电流-电压曲线上移,通道稳态激活曲线右移,通道稳态失活曲线左移,但恢复时间不变。预先给予7 μmol/L的PIP可明显减轻H2O2对APD、ICa,L的抑制作用(P<0.01),对L型钙通道动力学的异常影响。结论:PIP可减轻氧化应激对心房肌细胞APD、ICa,L的影响。     

Altered transient outward current in human atrial myocytes of patients with reduced left ventricular function

INTRODUCTION: Electrophysiologic remodeling is involved in the self-perpetuation of atrial fibrillation. To define whether differences in atrial electrophysiology already are present in patients with increased susceptibility for atrial fibrillation, we compared patients in sinus rhythm with and without heart failure. METHODS AND RESULTS: Atrial specimens were obtained from patients with reduced left ventricular ejection fraction (LVEF; n = 10) and normal LVEF (n = 16) who were undergoing aortocoronary bypass surgery and from donor hearts (n = 4). Enzymatically isolated atrial myocytes were investigated by whole cell, patch clamp techniques. Total outward current was significantly larger in myocytes of hearts with low LVEF than normal LVEF (19.4 +/- 1.3 vs 15.1 +/- 1.2 pA/pF at pulses to +60 mV, respectively). Analysis of inactivation time courses of different outward current components revealed that the observed current difference is due to the transient calcium-independent outward current I(to1) which is twice as large in the low LVEF group than in the normal LVEF group (9.4 +/- 0.9 vs 4.7 +/- 0.4 pA/pF at pulses to +60 mV, respectively). I(to1) recovery from inactivation was significantly more rapid in myocytes of hearts with low LVEF, and action potential plateau in these cells was significantly shorter. The results of I(to1) and action potential measurements in atrial myocytes of donor hearts were very similar to the results of patients with preserved heart function. CONCLUSION: I(to1) in human atrial myocytes of patients with reduced LVEF has an increased density and altered kinetics in sinus rhythm. These differences in outward current may explain the reduced plateau phase of action potentials.     

缺血/再灌注对心肌细胞瞬间外向钾电流的影响

目的探讨在心肌缺血/再灌注后,瞬间外向钾电流（transientoutsidepotassiumcurrent,Ito）的变化及其在室性心律失常发生中的作用。方法以常规方法制备大鼠心肌缺血/再灌注模型,以酶解法分离单个心室肌细胞,采用全细胞膜片钳记录技术观察缺血10min和30min后,再灌注组的心室肌细胞Ito的变化,以正常心肌的Ito为对照组。结果缺血/再灌注组心室肌细胞Ito电流密度$C电压关系曲线下移,+70mV的Ito密度对照组为52.2±12.1pA/pF（n=11cells）,缺血10min和30min再灌注组分别为7.2±2.5pA/pF（n=9cells）和6.4±2.7pA/pF（n=10cells）,与对照组相比有显著性差异（P<0.01）。其失活曲线右移,半数最大失活电位对照组为-60±14mV（n=9cells）,缺血10min和30min再灌注组分别为-58±12mV（n=8cells）和-50±12mV（n=9cells）,与对照组比较,缺血30min再灌注组显著减小（P<0.05）,而缺血10min再灌注组变化不明显（P>0.05）。缺血10min再灌注组Ito失活后再恢复过程较对照组显著减慢（P<0.05）,而缺血30min再灌注组有恢复趋势。结论缺血/再灌注心室肌细胞瞬间外向钾电流受抑制,可能为缺血/再灌注性心律失常发生的机制之一。     

马钱子碱对大鼠心室肌细胞瞬时外向钾电流的影响

目的:探讨马钱子碱(brucine)对大鼠心室肌细胞瞬时外向钾电流(transient outward potassium current,Ito)及其动力学的影响。方法:用酶解法分离大鼠单个心室肌细胞。用全细胞膜片钳技术记录不同浓度的马钱子碱可对大鼠心室肌细胞Ito的前后影响变化。结果:①马钱子碱可浓度依赖性地阻断Ito;②5μmol/L的马钱子碱可使Ito稳态激活曲线右移,V1/2由对照的(-30.7±10.2)mV变为(-27.8±5.8)mV(P0.05);③5μmol/L的马钱子碱可使Ito稳态失活曲线左移,V1/2分别为(-41.6±1.0)mV变为(-75.0±2.8)mV(P0.05);④5μmol/L的马钱子碱可使Ito稳态激活曲线右移失活后再恢复时间常数τ延长。结论:提示马钱子碱可以阻断Ito,对Ito的激活态和失活态均具有较高的亲和力,这些可能是其抗心律失常作用的机制。     

Reduced Inward Rectifying and Increased E-4031-Sensitive K+ Current Density in Arrhythmogenic Subendocardial Purkinje Myocytes from the Infarcted Heart

Outward Currents in Purkinje Cells from 48-Hour Infarcted Heart. Introduction : Subendocardial Purkinje myocytes from the 4K-hour infarcted heart (IZPCs) have reduced resting potentials, possibly due to altered inwardly rectifying K⁺ currents I_KI. Abnormal depolarization-activated outward K⁺ currents could contribute to long triangularly shaped action potentials of IZPCs.
Methods and Results : We used whole cell patch recordings to compare cesium-sensitive I_KI and 4-aminopyridine (4-AP)-resistant, noninactivating sustained I_K between normal Purkinje myocytes (NZPCs) and IZPCs. IZPCs showed decreased net membrane currents. Two IZPC groups were distinguished, based on 4-AP-resistant outward K⁺ currents. IZPC-I had isochronal I_KI current-voltage relations similar to NZPCs whereas IZPC-II showed significantly reduced I_KI and increased outward plateau currents. To study the sustained I_K in the presence of the Class III antiarrhythmic agent E-4031, a two-pulse protocol was used to inactivate transient outward currents, followed by step depolarizations. E-4031-sensitive currents were significantly greater in IZPCs at depolarized potentials (> 0 mV). Similar to NZPCs, IZPC E-4031 currents showed time dependence during depolarization, lack of rectification at positive steps, and voltage-dependent recovery from block.
Conclusion : Decreased I_KI may account for reduced resting potentials in IZPCs. E-4031-sensitive currents in NZPCs, unlike those in canine ventricular myocytes, are sensitive to 4-AP and are larger in IZPCs.     

Effects of angiotensin II on membrane current in cardiac Purkinje fibers

We studied the actions of the octapeptide hormone angiotensin II (AII) on isolated cardiac Purkinje fibers. AII (1 to 75 nm) increased the height and duration of the plateau phase of the action potential and increased the strength of contraction in these preparations. These effects were not blocked by propranolol (10^?6m). A two-microelectrode voltage clamp technique combined with simultaneous tension measurements was used to study the AII-induced changes in membrane current and contractile activation. AII enhanced peak tension and promoted an inward shift in the net membrane current-voltage relation at test voltages between ?40 and 0 mV. The inward shift in current was maintained for the duration of the 500 ms test voltage step. The AII-induced current shift was reduced or abolished when external calcium concentration was decreased from 5.4 mm to 1.8 mm, and was inhibited by the calcium antagonist D600.     

急性心肌梗死对心室肌细胞钾电流的影响

目的 :研究急性心肌梗死 （AMI）心室肌细胞瞬时外向钾电流 （Ito）和内向整流性钾电流 （IK1 ）的变化。方法 :采用结扎兔冠状动脉左前降支的方法建立 AMI动物模型 ,应用膜片钳全细胞记录方法 ,记录比较 AMI后 1周心外膜梗死区心肌细胞 Ito和 IK1 的变化。结果 :心梗组 Ito明显下降 ,I- V曲线明显下移。指令电位为 +60 m V时 ,Ito在心梗组为 1.0 8± 0 .2 4n A（n=12 ） ,与对照组 （2 .0 9± 0 .3 9n A ,n=16）相比 ,显著下降 ,P<0 .0 1;心梗组 IK1 与对照组比较 ,明显下降 ,特别在超极化时。指令电位为 - 12 0 m V时 ,心梗组 IK1 为 3 .0 1± 0 .49n A （n=11） ,对照组为 4.12±0 .5 1n A（n=10 ,P<0 .0 5 ）。结论 :AMI可引起心室肌细胞 Ito和 IK1 的下降 ,从而导致动作电位平台期延长、复极异常 ,这可能是导致 AMI后出现折返性室性心律失常的原因     

Effect of lidocaine on the early inward transient current in sheep cardiac Purkinje fibers.

We used two experimental techniques to study the effect of lidocaine hydrochloride on the early inward transient (sodium) current as it is reflected by the maximum rate of change of action potential phase 0 (Vmax). We assessed the effect of lidocaine on Vmax as Purkinje fibers were slowly depolarized by increasing the extracellular potassium concentration from 4.0 to 16.0 mM; these voltage-dependent effects were compared with lidocaine's effect on membrane responsiveness (which measures both the time and the voltage dependence of Vmax). We also used a voltage clamp technique to establish the effect of lidocaine on the voltage dependence of Vmax by measuring Vmax 800-1000 msec after transmembrane voltage (Vm) had been changed in small steps. We studied the effect of lidocaine on the time course of early inward transient current reactivation by depolarizing the membrane to -25 +/- 5 mv for 100 msec to inactivate this current, clamping Vm to a repolarized test voltage for various periods, and then measuring phase 0 Vmax of action potentials elicited immediately after termination of the voltage clamp. We showed that lidocaine at 5 mg/liter, but not a 1 mg/liter, shifted the steady-state Vmax- Vm relationship to a more negative position on its voltage axis by about 5 mv and markedly slowed the reactivation of the measure early inward transient current.     

正常大鼠心室肌细胞动作电位和瞬时外向钾离子流的特点

目的研究正常Spraque-Dawley大鼠外层、中层和内层心室肌细胞动作电位(AP)和瞬时外向钾离子流(Ito)的特点。方法采用酶消化法获得大鼠外层、中层和内层心室肌细胞,以全细胞膜片钳技术记录心室肌细胞AP和Ito。结果成功记录到大鼠心室肌细胞外、中和内层心肌细胞AP和Ito。外层至内层心室肌细胞动作电位时程(APD)逐渐延长(P<0.05)。在+70mV刺激时外层至内层心室肌细胞Ito电流密度逐渐减小,分别为59.50±15.99,29.15±5.53和12.29±3.62pA/pF(P<0.05)。三层心室肌细胞曲线半激活电压、半失活电压及失活后恢复时间均无差异(P>0.05)。结论大鼠三层心室肌细胞AP形态和Ito大小存在分层差别。     

Ionic currents and action potentials in rabbit,rat, and guinea pig ventricular myocytes

Summary Distinct differences exist in action potentials and ionic currents between rabbit, rat, and guinea pig ventricular myocytes. Data obtained at room temperature indicate that about half of the rabbit myocytes show prominent phase 1 repolarization and transient outward current. Action potentials in guinea pig ventricular myocytes resemble those from rabbit myocytes not exhibiting phase 1 repolarization; and guinea pig myocytes do not develop transient outward current. Rat ventricular action potentials are significantly shorter than those from rabbit and guinea pig ventricular myocytes. Unlike rabbit and guinea pig myocytes, rat ventricular myocytes also exhibit a prominent phase 1 and lack a well defined plateau phase during repolarization. All rat ventricular myocytes exhibit a transient outward current which can be best fitted by a double exponential relation. There are no significant differences between the amplitude, voltage dependence and inactivation kinetics of the inward calcium currents observed in rabbit, rat and guinea pig. The steady-state current-voltage relations between –120 mV and –20 mV, which mostly represent the inward rectifier potassium current are similar in rabbit and guinea pig. The amplitude of this current is significantly less in rat ventricular myocytes. The outward currents activated upon depolarization to between –10 and +50 mV are different in the three species. Only a negligible, or absent, delayed rectifier outward current has been observed in rabbit and rat; however, a relatively large delayed rectifier current has been found in guinea pig. These large interspecies variations in outward membrane currents help explain the differences in action potential configurations observed in rabbit, rat, and guinea pig.     

瞬时外向钾电流及通道异常致心力衰竭心律失常的研究进展

慢性心力衰竭恶性心律失常发病率、致死率高,严重影响心力衰竭患者生活质量。心肌细胞离子通道异常导致动作电位时程(APD)延长,进而诱发异常触发活动是心力衰竭心律失常发生的主要机制。瞬时外向钾电流(I_to)主要参与心肌细胞动作电位(AP)的1期复极,对心力衰竭时APD延长具有重要作用;钾通道相互作用蛋白2(KChIP₂)是I_to通道上的的重要功能亚单位,对I_to具有关键性调控作用,KChIP₂基因敲除大鼠心肌细胞I_to几乎完全消失,心律失常易感性显著增加。本文对慢性心力衰竭心律失常的钾离子通道机制研究进展进行综述,以期为心力衰竭心律失常的治疗靶点提供思路。     

卡托普利对豚鼠心室肌细胞动作电位及外向延迟整流钾电流的作用

目的 探讨卡托普利对豚鼠心室肌细胞动作电位及外向延迟整流钾电流的作用。方法 采用内充3M KCL的标准微电极记录心肌动作电位。采用膜片钳全细胞技术，钳制电位-50mV，持续时间100ms，指令电位 40mV，记录外向延迟整流钾电流(Ik)最大峰电流。结果 与缺血组比较，卡托普利组APD30、APD50及ERP显著延长，APD50无显著变化。缺血组Ik幅度显著增高，而卡托普利组及卡托普利 缺血组显著降低。各组电流—电压关系曲线形态虽无显著变化，但缺血组显著上移，而卡托普利组、卡托普利 缺血组比缺血组下移。结论卡托普利降低外向钾电流及延长APD30、APD50和ERP。