利多卡因对兔心室肌细胞动作电位的影响及对快钠电流的阻滞作用

目的探讨利多卡因对心室肌细胞动作电位(AP)的影响以及对快钠电流(INa-T)的张力性阻滞和使用依赖性阻滞作用。方法急性分离新西兰大白兔心脏,并予消化酶消化获得单个心室肌细胞,采用微电极技术检测AP相关参数:最大舒张期电位、零相最大上升速率(Vmax)、AP振幅,以及复极化20%、50%和90%时的AP时程(APD_(20)、APD_(50)、APD_(90))。采用全细胞膜片钳技术检测兔心室肌细胞的INa-T。用100μmol/L利多卡因溶液灌流干预,观察各参数的变化。结果100μmol/L利多卡因灌流后,兔心室肌细胞最大舒张电位无明显变化[(-81±7)m V比(-80±6)m V,P=0.102],AP振幅显著降低[(100±12)m V比(127±9)m V,P=0.002],Vmax明显减慢[(328±41)V/s比(422±45)V/s,P=0.004],APD_(90)显著缩短[(66±8)ms比(85±10)ms,P=0.021],峰值钠电流明显降低[(2 468±389)p A比(3 223±367)p A,P=0.003]。在5 Hz频率刺激下,利多卡因灌流前第40个刺激与第1个刺激诱发的电流分别为(3 145±323)p A和(3 287±432)p A(P=0.087),灌流后电流分别为(1 125±298)p A和(2 365±376)p A(P=0.013)。结论利多卡因降低AP振幅,减慢Vmax,缩短APD90,对INa-T不但有张力性阻滞,更有显著的使用依赖性阻滞作用。     

普罗帕酮对兔心室肌细胞INa-T的张力性阻滞和使用依赖性阻滞

目的 探讨普罗帕酮对兔心室肌细胞瞬时钠电流（INa-T）的张力性阻滞和使用依赖性阻滞作用。方法 采用全细胞膜片钳技术检测兔心室肌细胞INa-T的I-V曲线及不同频率下的峰值电流，并用10 μmol/L普罗帕酮溶液灌流干预。 结果 普罗帕酮灌流后INa-T的I-V曲线明显上移，峰值电流显著下降〔(3001±383) pA vs.(4193±378) pA，P<0.05〕。以0.06 Hz和1Hz频率刺激时，普罗帕酮未显示使用依赖性阻滞作用。当以2 Hz、5 Hz和10 Hz频率刺激时，阻滞率分别为（22±11）%、（38±14）%和（52±17）%，3组间两两比较以及与对照组和普罗帕酮在0.06 Hz和1 Hz时的阻滞率的差异有显著统计学意义(P<0.05)。结论 普罗帕酮对INa-T不但有张力性阻滞作用，也有显著的使用依赖性阻滞作用。     

普罗帕酮对兔心室肌细胞Ⅰ_(Na-T)的张力性阻滞和使用依赖性阻滞

目的探讨普罗帕酮对兔心室肌细胞瞬时钠电流(Ⅰ_(Na-T))的张力性阻滞和使用依赖性阻滞作用。方法采用全细胞膜片钳技术检测兔心室肌细胞Ⅰ_(Na-T)的Ⅰ-Ⅴ曲线及不同频率下的峰值电流,并用10μmol/L普罗帕酮溶液灌流干预。结果普罗帕酮灌流后Ⅰ_(Na-T)的Ⅰ-Ⅴ曲线明显上移,峰值电流显著下降〔(3001±383)pA vs.(4193±378)p A,P0.05〕。以0.06 Hz和1Hz频率刺激时,普罗帕酮未显示使用依赖性阻滞作用。当以2 Hz、5 Hz和10 Hz频率刺激时,阻滞率分别为(22±11)%、(38±14)%和(52±17)%,3组间两两比较以及与对照组和普罗帕酮在0.06 Hz和1 Hz时的阻滞率的差异有显著统计学意义(P0.05)。结论普罗帕酮对Ⅰ_(Na-T)不但有张力性阻滞作用,也有显著的使用依赖性阻滞作用。     

胺碘酮慢性作用对兔心室肌细胞L型钙通道电流和跨壁动作电位相关性研究

目的 从单个心室肌细胞L型钙通道电流时间常数(τ)和组织块跨壁动作电位复极90%时程(APD90),探讨胺碘酮慢性作用抗心律失常的可能细胞电生理机制.方法 健康兔口服胺碘酮80 mg·kg-1·d-1共4周,记录离体兔带血管心室肌组织块跨膜心室肌细胞动作电位后分离心室肌细胞,记录单细胞L型钙通道电流τ,比较对照组、胺碘酮组及索他洛尔组干预下τ与APD90比值(τ/APD90)变化.结果 对照组τ为(98±8)ms(n=10)、APD90为(220±10)ms(n=5)、τ/APD90为0.44±0.03.与对照组相比,胺碘酮组τ明显延长[为(164±8)ms,n=8,P＜0.05],APD90亦明显延长[为(321±12)ms,n=5,P＜0.05],τ/APD90较对照组增加(分别为0.51±0.03与0.44±0.03,P＜0.05).索他洛尔(3×10-5mmoL/L)组与对照组相比,τ明显延长[为(128±7)ms,n=8,P＜0.05],但因APD90延长较著[为(405±13)ms,n=4,P＜0.01],使τ/APD90较对照组明显减少(分别为0.32±0.05与0.44±0.03,P＜0.05).索他洛尔+胺碘酮组的τ为(150±12)ms、APD90为(355±11)ms(n=4),与索他洛尔组比较,τ/APD90增加(为0.44±0.02,P＜0.05),与对照组相比,差异无统计学意义(P＞0.05).结论 心室肌细胞膜L型钙通道电流的τ/APD90大小与胺碘酮慢性作用相关,这为胺碘酮慢性作用的安全性提供了一种可能解释.     

L型钙通道在LQTl发病机制中作用的实验研究

目的 分析L型钙电流(IcaL)在犬三层心室肌细胞中的特点,探讨其在LQTl发病机制中的作用.方法 成年杂种犬14只,体重13～15 kg,雌雄不拘.分离犬三层心室肌细胞,采用全细胞膜片钳技术记录动作电位(AP)和ICaL,依次用Chromanol 293B(50ìμmoL/L)阻断慢激活延迟整流性钾电流(IKs)模拟LQTl,用异丙肾上腺素(100 nmo/L)激活13肾上腺素受体(β-AR),观察AP和,ICaL的变化.分三层取少量心室肌组织,采用实时定量逆转录聚合酶链反应(RT-PCR)技术,检测各层L型钙通道a1C亚单位的mRNA含量.结果 正常情况下,犬三层心室肌细胞ICaL电流密度差异无统计学意义[外层(4.253±0.782)pA/pF,中层(4.392±0.714)pA/pF,内层(4.182±0.665)pA/pF,P＞0.05],而中层心室肌细胞动作电位时限(APD)较内层和外层的长[外层(721.48±26.59)ms,中层(911.80±31.24)ms,内层(783.52±25.27)ms,P＜0.05];阻断IKs后ICaL电流密度没有变化,而APD均明显延长[(外层(835.21±27.34)ms,中层(1089.21±30.55)ms,内层(830.64±27.12)ms,与阻断IKs前相比,P＜0.05)];β-AR兴奋使三层心室肌细胞ICaL显著增加,且三者变化差异无统计学意义[(外层(5.654±0.756)pA/pF,中层(5.458±0.702)pA/pF,内层(5.600±0.819)pAZpF,P＞0.05].但β-AR兴奋使外层和内层心室肌细胞APD缩短,中层心室肌细胞APD延长,三者变化差异有统计学意义[外层(792.63±26.71)ms,中层(1127.85±32.10)ms,内层(811.32±27.52)ms,P＜0.05].实时定量RT-PCR结果显示,三层心室肌细胞中alC亚单位的mRNA含量差异无统计学意义(外层0.112±0.019,中层0.077±0.018,内层0.109±0.012,P＞0.05).结论 L型钙通道在犬三层心室肌中的分布没有差异,在LQTl模型中,Iso使三层心室肌细胞,ICaL均匀增加,推测ICsL本身没有引起LQTl复极不稳定.     

艾司洛尔对心室肌细胞动作电位及L-型钙离子通道的影响

目的 观察艾司洛尔对豚鼠心室肌细胞动作电位(AP)和L-型钙离子通道的影响.方法 Langendorff离体心脏逆向灌流法分离豚鼠心室肌细胞,随机选取心室肌细胞分为正常对照组和艾司洛尔(50 μmol/L和100 μmol/L)组.应用全细胞电流钳模式记录心室肌细胞AP,应用电压钳模式记录L-型钙离子通道电流(ICa-L).结果 艾司洛尔(100 μmol/L )可使心肌细胞AP时程APD20、APD50明显缩短(P<0.05),心室肌细胞ICa-L峰值电流明显降低(P<0.05).结论 艾司洛尔缩短心室肌细胞AP时程和抑制钙通道可能是其抑制交感风暴的机制之一.     

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。     

低渗性肿胀对豚鼠心室肌细胞动作电位及延迟整流钾电流的影响

观察单个豚鼠心室肌细胞动作电位和主要复极期电流延迟整流钾电流(IK)的变化,探讨急性心肌缺血再灌注室性心律失常发生的离子机制。采用全细胞膜片钳记录技术,观察低渗液(200mOsm/kg)灌流胶原酶分离的单个豚鼠心室肌细胞发生肿胀后的动作电位各参数的变化,同时记录IK及其快、慢两种激活成分(IKr及IKs)的变化。结果:低渗液灌流后心室肌细胞迅速发生肿胀,动作电位幅度(APA)、静息膜电位(RMP)及阈电位水平无明显变化;而动作电位时程(APD)在600,1000和3000ms三种基础起搏周长(BCL)刺激时均缩短(P<0.05),尤以APD复极达50%和90%时缩短更为明显。APD生理性频率适应性消失且离散度增大。低渗性肿胀状态下IK电流幅度在3000ms长去极化保持时间(主要成分为IKs)刺激时从1134.33±150.17pA增加至1621.98±234.95pA(P<0.001,n=10);而在100ms短去极化保持时间(主要成分为IKr)刺激时从693.44±96.44pA降低至294.06±71.79pA(P<0.05,n=8);并且使IK的IV曲线向上移位。结论:低渗性肿胀的心室肌细胞IK特别是IKs的增加是引起APD缩短的重要因素,是急性心肌缺血再灌注室性心律失常发生的离子机制之一。     

普罗帕酮对心室间复极异质性影响的电药理学机制研究

目的观察普罗帕酮对生理状态下兔心肌心室间复极异质性的影响,从动作电位时程(action potential dura- tion,APD)的角度探讨临床应用普罗帕酮治疗心律失常作用的电药理学机制。方法采用膜片钳技术,观察在不同刺激频率[即基础循环周长(basic cycle length,BCL)=2000、1000、500及250ms]下,不同浓度普罗帕酮(对照组,1μmol/L普罗帕酮组,6μmol/L普罗帕酮组,10μmol/L普罗帕酮组)对正常心肌左右心室内膜APD的影响。结果普罗帕酮由低浓度(1μmol/L)至超治疗浓度(10μmol/L)呈非浓度依赖性地减少室间离散;左右心室内膜APD和室间离散在不同浓度的普罗帕酮干预下仍呈慢频率依赖性特点(P＜0．05),且这种特点对普罗帕酮呈非浓度依赖性。结论生理状态的心肌左右心室间存在复极离散。普罗帕酮可减少这种复极异质性,这可能是其对无缺血心肌室性心律失常治疗作用的电药理学机制之一。     

牵张刺激对乳大鼠心房肌细胞瞬时外向钾电流和动作电位的影响

目的:探究牵张刺激对乳大鼠心房肌细胞瞬时外向钾电流(Ito)和动作电位时程(APD)的影响。方法:1d龄SD乳鼠,采用胰酶消化法分离获得心房肌细胞。于细胞牵引装置培养24h分组:对照组:不予牵张刺激;牵张组:牵张增加12%硅胶膜面积24h。采用膜片钳全细胞记录方法记录两组细胞膜Ito和APD的变化。结果:在+20~+60mV刺激电压水平,牵张组Ito电流密度与对照组相比明显降低[(1.6±0.4)pA/pF∶(12.1±2.9)pA/pF,P0.01,n=9];牵张组动作电位复极50%(APD50)、复极90%(APD90)均明显缩短[(10.5±1.4)ms∶(15.5±2.4)ms,(30.0±2.8)ms∶(56.3±3.6)ms;均P0.01,n=9]。结论:牵张刺激可降低乳鼠心房肌细胞Ito电流密度,缩短APD,这可能是压力负荷增大致心房电重构的基础之一。     

An example of combined sinoatrial and atrioventricular block

Combined sinoatrial and atrioventricular block is rare and has been reported in patients on digitalis. We report a case of combined Mobitz type II sinoatrial block and 2:1 atrioventricular block in a patient on no medication who presented with recurrent syncope.     

Complete atrioventricular block during cardiac catheterization: Two case reports in patients without pre-existing conduction abnormalities

Third-degree atrioventricular block has been well documented during ventricular catheterization of patients with underlying conduction abnormalities. Two cases reported here describe patients with normal conduction at baseline who sustained complete heart block during ventricular catheterization. Catheterizing physicians should be aware of this risk, which has not been previously reported.     

Case Report: Type I Second-Degree AV Block Masquerading as Type II Block

This report describes a patient with type I second-degree atrioventricular block and sequences consistent with type II block according to widely accepted criteria. The electrocardiograms illustrate the importance of deductive reasoning and the clinical context in the diagnostic evaluation of perplexing forms of second-degree AV block.     

Occurrence of complete heart block associated with acute renal infarction

Complete heart block (CHB) and acute renal infarction (ARI) are both uncommon diseases and seldom encountered in the clinical practice. We describe a rare case of pre‐existing left bundle branch block, presenting simultaneously with CHB and ARI. The possible mechanism depends on prior presence of either CHB or ARI. If ARI occurs first, severe pain and embolism may enhance the vagal tone resulting in decrease in the heart rate and transient intraventricular conduction interruption, which subsequently causes CHB. The opposite scenario, CHB preceding ARI, is also possible. CHB can be physiologic and transient, with higher risk of development in the circumstance of pre‐existing conduction system disturbances. Patients with CHB are predisposed to formation of thrombi and thromboemboli, giving rise to ARI. In conclusion, awareness and timely identification of the clinical manifestations of these two diseases may facilitate early diagnosis and prompt management.     

Resumption of interatrial conduction after atrial premature beat in baseline interatrial aberrancy

Interatrial block (IAB) is a delay or blockage of interatrial conduction from the right atrium to the left atrium, causing prolongation of the P-wave duration on the electrocardiogram. This condition is unfortunately not uncommon in clinical practice, especially among the elderly. It is often overlooked because the P wave is small and abnormalities can be difficult to detect. An isolated IAB does not usually cause any abnormal symptoms and may not require any specific treatment. Nevertheless, a relationship between an IAB and other cardiovascular conditions including left atrial electromechanical dysfunction, atrial remodeling, atrial fibrosis, atrial fibrillation, and stroke has been reported. Early diagnosis of this condition is critical. This case report presents a functional interatrial block or interatrial aberrancy that returned to normal after an atrial premature complex where the interatrial conduction remained normal in subsequent beats.     

Apparent bradycardia-dependent right bundle branch block associated with atypical atrioventricular Wenckebach periodicity as a possible mechanism

The Holter monitor electrocardiogram was taken from a 15-year-old male athlete. Intermittent right bundle branch block frequently occurred at rest. When sinus cycles gradually lengthened, sinus impulses were conducted to the ventricles with right bundle branch block (RBBB) in succession. When, thereafter, sinus cycles gradually shortened, sinus impulses were conducted without RBBB. However, it seems that these findings do not show true bradycardia-dependent RBBB. Atypical atrioventricular Wenckebach periodicity was occasionally found in which sudden shift from the period of comparatively short PR intervals to the period of long PR intervals occurred. In the Wenckebach periodicity, when a QRS complex occurs after a much longer pause, RBBB was not found, while when it occurs after a much shorter period, RBBB was found. This suggests that this case may be apparent bradycardia-dependent RBBB, namely, a form of tachycardia-dependent RBBB. This is the first report suggesting apparent bradycardia-dependent bundle branch block associated with gradual lengthening of sinus cycles, as a possible mechanism.     

AV block. Which type and where?

An electrocardiogram (ECG) showing sinus tachycardia with sinus rate exceeding the ventricular rate suggesting atrio-ventricular (AV) block in a patient with old anterior wall infarction is presented. The presence of varying PR intervals, irregular RR intervals and P-QRS relationship not consistent with 2nd degree type 1 AV block was seen. The possible site(s) and degree of AV block in the case is discussed.     

Phase 4 paroxysmal AV block in a patient with scleroderma

A 72-year-old man with limited cutaneous systemic scleroderma was hospitalized for two episodes of witnessed syncope. The baseline 12-lead electrocardiogram was normal but on telemetry there were numerous episodes of paroxysmal AV block with asystolic periods of up to 7.5 s duration. Analysis of the rhythm strips revealed phase 4 intra-His bundle block characterized by critical P-P intervals that triggered the AV block, and a narrow range of junctional escape to subsequent P wave intervals that were required to release the AV block. A dual chamber pacemaker was implanted.     

The RR index test for the differentiation of atrioventricular nodal block from His--Purkinje block during incremental atrial pacing in patients with bifascicular block

AIMS: His—Purkinje block induced by incremental atrial pacingis highly predictive of an impending high degree atrioventricularblock in patients with bifascicular block. The His potentialis, however, sometimes not measurable or is lost in the ventriculardepolarization. The aim of this study was to evaluate whetherthe comparison of RR intervals before and after atrioventricularblock, induced by incremental atrial pacing, could differentiatebetween atrioventricular nodal and His—Purkinje blockin patients with bifascicular block. METHODS AND RESULTS: In 98 patients with bifascicular block, incremental atrial pacingwas performed as part of an invasive electrophysiological study.An ‘RR index’ was constructed by calculating thenumerical difference between the RR interval immediately beforeand after the atrioventricular block divided by the RR intervalimmediately before the pacing-induced block. Endocavitary recordingof the His bundle potential was used for defining the levelof atrioventricular block. The median RR index was 0·98(range 0·88–1·02) in recordings with His—Purkinjeblock and 0·49 (range 0·11–0·89)in recordings with atrioventricular nodal block (P<0·001).An RR index of 0·85 had a sensitivity of 100% and a specificityof 99% for the identification of atrioventricular block localizedto the His—Purkinje system. CONCLUSION: The use of an RR index is a helpful tool in the differentiationof His—Purkinje from atrioventricular nodal block in patientswith bifascicular block undergoing incremental atrial pacingas part of an invasive electrophysical study.