交感神经调节失衡与缺血性心律失常关系的研究

为探讨急性心肌缺血后 ,交感神经对心室肌不同部位复极时程的调节及其与缺血性心律失常的关系 ,制备兔急性心肌缺血模型 ,分离、结扎并剪断双侧颈迷走、心交感神经 ,电刺激心交感神经远端。心室复极时程以心外膜电图 (EPG)的QT间期及采用玻璃微电极技术记录的动作电位时程 (APD90 、APD50 )表示。结果 :交感神经刺激使正常心室肌不同部位的QT间期、APD90 、APD50 均有明显缩短 (P <0 .0 5 ) ;不同部位心肌复极时程对交感神经刺激的反应性没有明显区别。急性心肌缺血后 ,交感神经刺激使缺血区QT间期、APD90 明显缩短 ,而非缺血区则无明显变化 ;非缺血区的QT间期、APD90 对交感神经刺激的反应性较缺血区明显减小 (P <0 .0 5 )。心肌缺血后心室易损期明显延长 ,交感神经刺激后更为延长 (P <0 .0 5 )。结论 :急性心肌缺血后 ,交感神经对非缺血区心室复极的调节作用减弱 ,交感神经兴奋导致心肌复极的不同步性更进一步增加 ,心室易损性增加 ,引起缺血性心律失常。     

哌仑西平对兔急性心肌缺血心率变异与心电生理的影响

观察小剂量哌仑西平对兔急性心肌缺血时心率变异 (HRV)与心电生理的影响 ,为临床应用提供实验理论依据。建立兔急性心肌缺血模型 ,采用HRV的时域指标及频域指标测定心肌缺血时心脏自主神经功能 ,应用心电生理研究方法测定心肌缺血时的心室有效不应期 (VERP)、VERP离散度 (VERPD)、QT间期离散度 (QTd)、心室颤动阈值 (VFT)的变化 ,比较哌仑西平预处理组与对照组各项指标。结果 :兔急性心肌缺血时 ,与对照组比较 ,哌仑西平预处理组HRV时域指标RR间期 (2 85 .6± 16 .3vs 2 5 0 .9± 8.4ms)、SDNN(6 .0± 2 .6vs 3.9± 0 .9ms)、rMSSD(6 .3± 1.3vs 4.8± 0 .9u)、CV(% ) (2 .6± 0 .33vs 1.9± 0 .19)、HRVI(9.5± 1.8vs 5 .9± 1.0u)均增高 (P <0 .0 5 ) ;频域指标VLF(0 .12 5± 0 .0 16vs 0 .19± 0 .0 17ms2 )、LF(0 .46± 0 .0 3vs 0 .5 2± 0 .0 4ms2 )、LF/HF(0 .14± 0 .0 0 5vs 0 .34± 0 .0 12 )均降低(P <0 .0 5 ) ,HF(3.2± 0 .16vs 2 .1± 0 .12ms2 )增高 (P <0 .0 1) ;心电生理指标VERPD(14.4± 4.2vs 2 1.2 5± 5 .2ms)及QTd(2 9± 8vs 2 6± 9ms)降低 (P <0 .0 5 ) ,VFT(36 .5± 7.9vs 2 3.8± 7.4mA)增高 (P <0 .0 5 )。相关性分析显示HRV指标与VFT相关。结论 :小剂量哌仑西平预处理能改?     

程序电刺激时心室复极离散度的研究

了解程序电刺激 (PES)时心室复极离散度的变化 ,探讨PES诱发室性快速心律失常 (VTA)的可能机制。采用单相动作电位 (MAP)标测技术测定 10例无器质性心脏病的阵发性室上性心动过速患者接受PES时的心室复极离散度。结果 :S1 S1 刺激 ( 5 0 0ms)时的动作电位时程 (APD)的离散度 (APDd)与窦性心律时无明显差异 ( 34± 10msvs38± 9ms ,P >0 .0 5 )。随S1 S2 间期缩短 ,各标测点S2 的APD逐渐缩短 ,且与S1 S2 间期呈正相关 ,但激动时间 (AT)及其离散度 (ATd)、APDd、复极时间离散度 (RTd)逐渐延长 ;S1 S2 间期缩短至有效不应期 (ERP) +30ms后 ,S2 的APDd、RTd大于窦性心律及S1 S1 刺激时 (APDd :5 1± 8msvs 38± 9ms或 34± 10ms,P <0 .0 5 ;RTd :39± 10msvs2 4± 7ms,P<0 .0 5 ) ,但ATd无明显增大。心室内各点有效不应期离散度为 31± 14ms,ERP APD平均为 0 .89± 0 .0 8。认为在无器质性心脏病者PES可使心室复极离散度增大 ,但不增加传导差异 ,不易诱发VTA     

急性心肌缺血家兔心室易损期和心室颤动阈的变化

目的观察急性心肌缺血对心肌易损性的影响。方法采用程序电刺激方法测定家兔心室颤动阈(VFT)、心室易损期(VVP)和有效不应期(ERP)。结果 急性心肌缺血时VFT降低,VVP延长,ERP缩短。VFT的迅速降低发生于冠状动脉结扎1分钟左右,结扎5分钟VFT降低幅度最大,由对照值10.55±1.54V降为6.39±1.19V(P相似文献   

家兔心室肌各层细胞的动作电位及瞬间外向钾电流特性

研究心室肌各层细胞的动作电位 (AP)、瞬间外向钾电流 (Ito)特性、并探讨两者之间关系。采用膜片钳技术记录心室肌内膜、中层 (M细胞 )、外膜层细胞的Ito及苯巴比妥对其影响 ,并与AP复极化达 90 %时程 (APD90 )进行比较。结果 :M细胞AP呈尖峰 圆顶形并有切迹 ,且APD90 最长。使用苯巴比妥后心室肌三层细胞 (由内→外 )APD90 在30 0ms基础刺激周长 (BCL)下缩短了 11.3% ,19.4%和 31.2 % (P <0 .0 5 ) ;在 6 0 0 0msBCL下分别下降了 11.5 % ,31.2 %和 13.4% (P <0 .0 5 )。M细胞、外膜层细胞的Ito比内膜层细胞大 (14.85± 1.1PA·PF- 1 、15 .2± 2 .3PA·PF- 1 vs 8.30± 0 .5 5PA·PF- 1 ;P <0 .0 5 )使用苯巴比妥后心室肌三层细胞 (由内→外 )下降了 2 9.5 % ,46 .7% ,47.2 % (P <0 .0 5或0 .0 1)。结果提示Ito呈正向影响APD ,影响程度受基础频率和不同层次细胞的制约     

β受体激动剂对LQT1模型的电生理影响

目的探讨LQT1患者在交感神经兴奋时发生室性心律失常的机制。方法实验切取犬楔形心室肌组织块,用30μmol/L chromanol 293B(I_(Ks)阻断剂)灌流该标本模拟LQT1,采用玻璃微电极和特制的金属电极,同步记录造模前后的中层和外层心室肌细胞的跨膜动作电位(TAP)和跨壁心电图(TECG),并观察异丙肾上腺素(Iso,100 nmol/L)对造模后的TAP和TECG的影响。结果chro- manol 293B使中层和外层心室肌细胞动作电位时限(APD_(90))均匀延长[中层：(287±12)ms vs(362±18)ms,P＜0．05；外层：(229±13)ms vs(303±20)ms,P＜0．05],跨壁复极离散度(TDR)增加不明显[(46±5)ms v8(49±7)ms,P＞0．05],TECG示QT间期延长[(314±13)ms vs(389±16)ms,P＜0．05]。加入Iso后,中层心室肌细胞APD_(90)延长[(362±18)ms vs(388±14)ms,P＜0．05],并出现早期后除极(EAD),外层心室肌细胞APD_(90)缩短[(303±20)ms vs(285±12)ms,P＜0．05],TDR明显增加[(49±7)ms vs(87±11)ms,P＜0．05],TECG示QT间期延长[(389±16)ms vs(405±15) ms,P＜0．05],并能自发产生室性早搏和室性心动过速。结论在LQT1模型中,Iso对中层和外层心室肌细胞TAP的影响不一致,引起TDR增加,这可能是交感神经兴奋使LQT1患者发生室性心律失常的机制。     

急性心肌梗死患者心室复极变异研究

目的描述急性心肌梗死(AMI)患者24小时心室复极变异性。方法对65例AMI患者和80例正常人行24小时Holter检测,人工编辑QRS-T波群模板,计算机辅助测定QT间期、RR间期、QT变异度(QTV)、心率变异性SDNN,计算QT变异系数(QTCV)、及QT变异度指数(QTVI)。结果①AMI组较正常对照组平均心率减慢(68.02±12.01bpmvs.73.57±7.65bpm,P<0.01),平均QT间期延长(382.96±37.07msvs.367.66±25.58ms,P<0.05),而两组QTc无显著差异(405.13±19.87ms,vs.404.1±18.65ms,P>0.05)。②AMI组24hQTV和QTCV显著低于正常对照组(25.03±9.91msvs.29.95±7.27ms,P<0.01;0.066±0.03vs.0.081±0.02,P<0.01)。③AMI组24小时QTVI较正常组显著增高(-0.45±0.41vs.-0.76±0.25,P<0.01)。结论AMI患者较正常对照组全天QT变异度和QT变异系数显著降低,可能与交感神经受损、心率变异降低有关。去除心率变异影响后,AMI患者QT变异度指数增高,心室复极变异增大。推测AMI造成的心肌缺血和心肌坏死,导致心室复极变异增大。QTVI可能是一个新的AMI电生理紊乱预测指标。     

新生大鼠心肌细胞短暂外向钾电流下降与心肌肥大的相关性研究

在某些心力衰竭患者中常观察到心肌细胞短暂外向钾电流 (Ito)下降和动作电位时程 (APD)延长 ,笔者主要探讨Ito下降与心肌肥大的关系及内在机制。用Ito阻断剂 ,4 氨基吡啶 (4 AP) ,处理新生大鼠心室肌细胞 ,观察作为心肌肥大指标的细胞膜电容和3 H 亮氨酸 (3 H Leu)掺入量 ,同时测Ito振幅和APD。结果 :Ito振幅下降近 5 0 %(1 5 0 .3± 1 8.6pA ,n =7vs 74 .0± 1 1 .5pA ,n =1 1 ,P <0 .0 5 )。APD50 (5 0 %复极 )显著的延长 (75 .8± 1 4 .1ms,n =7vs2 0 1 .7± 2 3.5ms,n =1 1 ,P <0 .0 5 )。膜电容和3 H Leu掺入量分别增加 4 7%和 31 % (P均 <0 .0 5 )。L 型钙通道阻断剂维拉帕米 ,能抑制 4 AP诱导的APD延长以及膜电容和3 H 亮氨酸掺入量的增加。环孢素A(CsA)也可抑制 4 AP诱导的膜电容和3 H Leu掺入量的增加 ,但对APD影响不明显。结论 :Ito下降通过延长APD ,致细胞内钙增加 ,激活钙调神经磷酸酶反应途径 ,可能引起心肌肥大     

银杏叶提取物对模拟缺血条件下兔心室肌细胞动作电位及ATP敏感性钾通道的影响

研究银杏叶提取物 (EGb)对模拟缺血条件下兔心室肌细胞三磷酸腺苷敏感性钾通道电流 (IKATP)及跨膜动作电位时程 (APD)的影响 ,以探讨其抗缺血性心律失常作用的电生理机制。采用酶解法分离获取兔心室肌细胞 ,将其分为正常对照、持续缺血、缺血预处理以及含EGb液 (15 ,30 ,6 0 ,12 0 μg/L)灌流 4组。用全细胞膜片钳技术 ,记录不同条件下的IKATP和跨膜动作电位。结果 :①与持续缺血组比较 ,缺血预处理以及EGb(12 0 μg/L)可使单个心室肌细胞APD50 、APD90 明显缩短 (n =5 ,P <0 .0 5 )。EGb处理组与缺血预处理组相比较 ,对APD的影响无显著差异 ;②与持续缺血组比较 ,缺血预处理和EGb(12 0 μg/L)均可以使IKATP由 112 4± 15 3pA增至 344 0± 2 0 5和 2 95 9± 12 9pA(n =5 ,P <0 .0 5 ) ,使得IKATPI V曲线抬高 ;③增大的电流均可被Glibenclimide阻断。结论 :EGb可开放细胞膜ATP敏感性钾通道、缩短APD ,产生类似心肌缺血预适应的病理生理过程。     

迷走神经刺激和乙酰胆碱灌注对心房肌电生理特性的影响

研究在体情况下迷走神经刺激(VNS)和乙酰胆碱(Ach)灌注对心房肌不同部位的电生理影响,并探讨其诱发心房颤动(AF)的机制。10只杂种犬自身随机对照,运用单相动作电位(MAP)记录技术,同步记录10只开胸犬的右心耳(RAA)、高位右房(HRA)、低位右房(LRA)、左心耳(LAA)、高位左房(HLA)、低位左房(LLA)的MAP,分别给予切断迷走神经、VNS、Ach灌注(分别做为对照组、VNS刺激组、Ach灌注组)后,观察诱发AF的情况和动作电位时程APD50、APD90和APD离散(dAPD)的变化。结果:10只犬在VNS刺激和Ach灌注同时,右心耳单一刺激分别有7只和6只犬诱发AF;VNS明显缩短APD50、APD90,其中RAA缩短最明显(APD50从72±5ms到19±4ms,APD90从136±7ms到43±5ms,P<0.001);Ach灌注也明显缩短APD50和APD90,与VNS相比,LLA的APD90缩短更明显(47±6msvs62±8ms,P<0.01);VNS明显升高心房肌APD50和APD90的离散(17±5msvs7±3ms,25±7msvs8±5ms,P<0.01)。结论:VNS和Ach灌注可引起APD缩短和离散升高,但影响的部位和程度稍有差异,都易诱发AF。     

Electrophysiologic effects of nicorandil on the guinea pig long QT1 syndrome model

INTRODUCTION: The slow component of the delayed rectifier K+ current IKs modulates repolarization of the cardiac action potential (AP), and the loss of IKs is known to cause long QT1 (LQT1) syndrome by prolonging action potential duration (APD). In this study, we generated a guinea pig LQT1 syndrome model using the IKs blocker chromanol 293B and then assayed the electrophysiologic effects of the ATP-sensitive potassium channel IK,ATP opener nicorandil on this model. METHODS AND RESULTS: Transmembrane action potentials of perfused right ventricular papillary muscle preparations and both in vitro and in vivo ECGs of guinea pigs were recorded. Blockade of IKs by chromanol 293B (30 microM) prolonged the action potential duration at 90% repolarization (APD90) by 8.5% and QT interval by 16.5% of control values. In addition, proarrhythmic early afterdepolarizations (EADs) and ventricular fibrillation were observed. Venoinjection of chromanol 293B (1 mg/kg) revealed 10.9% QT prolongation. Nicorandil (5-30 microM) dose-dependently shortened APD90 under the control condition, whereas it reversed the AP prolongation effect of chromanol 293B by 7.4% at the 30 microM concentration. Moreover, nicorandil shortened QT intervals both in vitro and in vivo and displayed an inhibitory effect on EADs and ventricular fibrillation. CONCLUSION: The ATP-sensitive potassium channel opener nicorandil may be an effective drug in the therapy of LQT1 syndrome by shortening APD and the QT interval.     

L-type calcium current recovery versus ventricular repolarization: preserved membrane-stabilizing mechanism for different QT intervals across species

BACKGROUND: Long QT syndrome is associated with early after-depolarization (EAD) that may result in torsade de pointes (TdP). Interestingly, the corrected QT interval seems to be proportional to body mass across species under physiologic conditions. OBJECTIVE: The purpose of this study was to test whether recovery of L-type calcium current (I(Ca,L)), the primary charge carrier for EADs, from its inactivated state matches ventricular repolarization time and whether impairment of this relationship leads to development of EAD and TdP. METHODS: Transmembrane action potentials from the epicardium, endocardium, or subendocardium were recorded simultaneously with a transmural ECG in arterially perfused left ventricular wedges isolated from cow, dog, rabbit, and guinea pig hearts. I(Ca,L) recovery was examined using action potential stimulation in isolated left ventricular myocytes. RESULTS: The ventricular repolarization time (action potential duration at 90% repolarization [APD(90)]), ranging from 194.7 +/- 1.8 ms in guinea pig to 370.2 +/- 9.9 ms in cows, was linearly related to the thickness of the left ventricular wall among the species studied. The time constants (tau) of I(Ca,L) recovery were proportional to APD(90), making the ratios of tau to APD(90) fall into a relatively narrow range among these species despite markedly different ventricular repolarization time. Drugs with risk for TdP in humans were shown to impair this intrinsic balance by either prolongation of the repolarization time and/or acceleration of I(Ca,L) recovery, leading to the appearance of EADs capable of initiating TdP. CONCLUSION: An adequate balance between I(Ca,L) recovery and ventricular repolarization serves as a "physiologic stabilizer" of ventricular action potentials in repolarization phases.     

胺碘酮对肥厚心肌钙调蛋白激酶活性的影响

目的观察口服胺碘酮对肥厚心肌细胞钙调蛋白激酶(CaMK)活性的影响,探讨胺碘酮抗心律失常的作用机制。方法30只家兔随机分为假手术组、心肌肥厚组和胺碘酮组,每组10只,喂养3个月,制备兔左室楔形心肌块。同步记录楔形心肌块容积心电图和内、外膜心肌细胞跨膜动作电位(TAP),程序电刺激诱发室性心律失常,并观察各组QT间期、跨室壁复极离散度(TDR)、早期后除极(EAD)和尖端扭转型室性心动过速(Tdp)的诱发率。利用放射免疫法测定心肌细胞CaMK活性。结果胺碘酮组和心肌肥厚组QT间期、内外膜心肌细胞TAP复极90%时程(APD90)和TDR均较假手术组明显延长(P<0.01),胺碘酮组QT间期和内、外膜心肌细胞APD90与心肌肥厚组相比进一步延长(P<0.05),但对TDR无明显影响。与假手术组比较,心肌肥厚组EAD和Tdp的发生率较假手术组明显升高(P<0.01),胺碘酮组EAD和Tdp的发生率较心肌肥厚组降低(P<0.05)。心肌肥厚组心肌细胞CaMK活性较假手术组明显升高,胺碘酮组CaMK活性较心肌肥厚组降低(P均<0.05)。结论胺碘酮抗心律失常的作用机制可能部分与抑制CaMK活性有关。     

Coexistence of two types of ventricular fibrillation during acute regional ischemia in rabbit ventricle

INTRODUCTION: We previously reported that a normal ventricle can demonstrate two types of ventricular fibrillation (VF), depending on the underlying electrophysiologic characteristics at the time of VF induction. We hypothesize that the two types of VF can coexist in acutely ischemic ventricles. METHODS AND RESULTS: Optical mapping studies were performed with di-4ANEPPS in 15 Langendorff-perfused rabbit hearts. Coronary artery branches were ligated to create regional ischemia in 10 hearts. Action potential duration measured to 50% repolarization (APD50) during ischemia showed an area with uniformly shortened APD50 (zone 1), an area with normal or lengthened APD50 (zone 3), and an area in between with an APD50 gradient (zone 2). Ischemia flattened APD restitution (APDR) slope and reduced conduction velocity in zone 1, creating a condition for type II VF. APDR steepened and the conduction velocity changed little in the nonischemic zone (zone 3), creating a condition for type I VF. During induced VF, the dominant frequency in zones 2 and 3 progressively increased after ischemia onset. The dominant frequency in zone 1 (ischemic zone) first decreased and then slightly increased but typically remained less than the dominant frequency in zone 3. The number of wavebreaks increased with time in all three zones (baseline: 4.3 +/- 1.5; 30 min: 11.7 +/- 5.6; 60 min: 15.6 +/- 11 per frame; P < 0.01). CONCLUSION: Two types of VF can coexist during acute regional ischemia. Both ischemic and nonischemic regions develop proarrhythmic changes during regional ischemia, thus contributing to increased ventricular vulnerability to VF and sudden death during acute coronary occlusion.     

Transmural action potential repolarization heterogeneity develops postnatally in the rabbit

INTRODUCTION: In the hereditary long QT syndrome, arrhythmia risk changes with age despite the presence of an ion channel mutation throughout development. Age-dependent changes in the transmural dispersion of repolarization may modulate this vulnerability. We recorded cardiac action potentials in infant, periadolescent, and adult rabbit myocardium to determine if transmural heterogeneities in repolarization are developmentally determined. METHODS AND RESULTS: Arterially perfused ventricular preparations were studied from 2-week (n = 7), 7-week (n = 7), and adult (n = 6) NZW rabbits. Action potentials were recorded with microelectrodes in five regions: epicardium (epi), subepicardium (subepi), midwall (mid), subendocardium (subendo), and endocardium (endo) during endocardial S1 pacing at cycle lengths of 2,000, 1,000, and 500 ms. At 2 weeks, the transmural APD90 profile was flat. With age, APD prolongation from subepi to endo created a transmural repolarization gradient. At 7 weeks, APD90 was significantly longer at subendo [204 +/- 2 ms (mean +/- SE) 2,000-ms cycle length, P < 0.05] vs both endo (193 +/- 2 ms) and epi (172 +/- 2 ms), causing a heterogeneous transmural APD90 gradient. In adults, the transmural gradient was a smooth continuum such that APD was shortest in epicardium and longest in endocardium. CONCLUSION: The transmural distribution of APD is developmentally determined. Tissue-specific age-dependent changes in APD can result in transmural repolarization heterogeneity. These age-related effects may modulate arrhythmia vulnerability during development.     

Ventricular fibrillation and shortening, alternans and after-depolarizations of epicardial monophasic action potentials during coronary occlusion and reperfusion: effect of repetition of ischemia

The relationship between the occurrence of ventricular fibrillation (VF) and repolarization abnormalities of the ischemic and reperfused myocardium is poorly understood. The present study examined the temporal relationship between ischemia- and reperfusion-induced changes in monophasic action potential (MAP) configurations and the occurrence of VF, and assessed the effects of repetition of ischemia. The left anterior descending coronary artery of 32 anesthetized dogs was occluded twice for 5 min, 30 min apart, during constant atrial pacing while recording MAPs from the epicardial ischemic zone. During the first occlusion, shortening of the MAP duration at 90% repolarization (APD90) and an increase in MAP alternans, defined as the maximal difference in APD90 between 2 consecutive beats, were observed. Afterdepolarizations also occurred transiently in 35% of the animals during occlusion and in 29% upon reperfusion. VF occurred in 28% (9/32 of the dogs) during the first sequence, and the incidence was higher in the subgroups with maximal alternans > or =20 ms (p<0.05), maximal shortening rate > or =30%, and afterdepolarizations. During the second sequence, the incidence of VF was reduced to 9% (3/32, p<0.05), associated with a significant reduction in the MAP changes. Thus, repolarization abnormalities of the ischemic and reperfused myocardium appear to be related to the occurrence of VF. The amelioration of the repolarization abnormalities by repetition of ischemia may be involved in its antifibrillatory effect.     

Sympathetic modulation of the relation between ventricular repolarization and cycle length

Sympathetic influences on ventricular repolarization are not yet fully elucidated, despite their relevance to arrhythmogenesis. The sympathetic control of repolarization, measured from an endocardial monophasic action potential duration (APD) and from the QT interval, was investigated in 24 anesthetized cats. The effects of right and left stellectomy and of subsequent bilateral stellectomy or beta-blockade on the relation between APD (or QT) and cycle length (CL) at steady state, and on the kinetics of adaptation of APD to a sudden change in cycle length were studied separately. Steady-state APD/CL (or QT/CL) relations were obtained by atrial pacing at different cycle lengths. The kinetics of APD adaptation were evaluated for a sudden decrease of approximately 100 msec in pacing cycle length. The steady-state APD/CL (QT/CL) relation was fitted by the hyperbolic function APD = CL/[(a. CL) + b]. From this, two parameters were computed: 1) 1/a, that is, APD (QT) extrapolated at infinite cycle length (APDmax or QTmax) and 2) the cycle length at which 50% of the total change in APD (or QT) occurred (CL50 = b/a). Right stellectomy reduced APDmax and CL50, an effect reversed by subsequent left stellectomy or beta-blockade (propranolol, 0.5 mg/kg). Left stellectomy prolonged APDmax and CL50. Bilateral stellectomy, in both groups, caused a further increase in these variables. Results were similar for the QT/CL relation. The adaptation kinetics of APD to cycle length was described by the sum of two exponentials. The first time constant (tau fast, about three beats) was unchanged by any intervention; the second (tau slow) was shortened by right stellectomy and prolonged by left stellectomy. The further removal of the remaining stellate ganglion had the same effect in both groups, that is, an increase in tau slow. Thus, sympathetic innervation modulates both the steady-state dependence on cycle length and the kinetics of adaptation to sudden rate changes of ventricular repolarization. The effects of sympathetic influence are asymmetrical. Right stellectomy shortens APDmax and QTmax, reduces CL50, and accelerates APD adaptation to a new steady state. Because these effects are reversed by beta-blockade or left stellectomy, they are likely to be due to a reflexly enhanced sympathetic outflow to the ventricles through the left-sided nerves.     

门冬氨酸钾镁对肥厚心肌室性心律失常的抑制作用

目的:观察口服门冬氨酸钾镁对肥厚心肌室性心律失常的影响并探讨门冬氨酸钾镁抗心律失常的作用机制。方法:将家兔随机分为假手术组、心肌肥厚组和门冬氨酸钾镁组。假手术组开腹但不行腹主动脉缩窄术,心肌肥厚组和门冬氨酸钾镁组采用腹主动脉缩窄术制备家兔心肌肥厚模型,喂养8周,制备兔左心室楔形心肌块,利用浮置玻璃微电极法同步记录楔形心肌块跨壁心电图和内、外膜心肌细胞跨膜动作电位,观察各组QT间期和内、外膜心肌细胞跨膜动作电位以及跨室壁复极离散度(TDR),程序电刺激诱发室性心律失常,记录早期后除极(EAD)和尖端扭转型室性心动过速(TDP)的诱发率。结果:门冬氨酸钾镁组和心肌肥厚组QT间期和内、外膜心肌细胞跨膜动作电位复极90%时程(APD90)和TDR较假手术组明显延长(均P<0.01)。门冬氨酸钾镁组与心肌肥厚组相比以上各项指标均明显缩短(均P<0.05)。假手术组、心肌肥厚组和门冬氨酸钾镁组EAD的发生率分别为0、100%和50%,TDP的发生率分别为0、40%和10%。心肌肥厚组与假手术组相比差异有统计学意义(P<0.01),门冬氨酸钾镁组与心肌肥厚组相比EAD和TDP的发生率明显降低(P<0.01)。结论:肥厚心肌TDR增大,心律失常的发生率显著升高。门冬氨酸钾镁降低TDR,可明显降低EAD和TDP的发生率。     

Developmental changes of cardiac repolarization in rabbits: implications for the role of sex hormones

OBJECTIVES: Firstly, to compare gender-dependent differences of cardiac repolarization in both adult and young rabbits. Secondly, to analyze the effect of gonadectomy on these gender differences in cardiac repolarization. METHODS: We evaluated potential gender differences in cardiac repolarization with both microelectrode and ECG recordings. QT(end), JT(end), and T(peak-end) intervals and action potential durations at 30%, 50% and 90% of full repolarization were used to assess ventricular repolarization in adult (normal and gonadectomized) and young rabbits of both sexes. RESULTS: Adult rabbits exhibited clear gender-related differences in repolarization evidenced by significantly longer JT(end) and T(peak-end) intervals and significantly longer APD30, APD50 and APD90 in females. These gender-related differences in repolarization were absent in young rabbits and were abolished by gonadectomy. CONCLUSIONS: Developmental changes of repolarization are present in rabbits. These changes are in agreement with those reported in humans and may further support the role played by sex hormones in the modulation of cardiac repolarization.