The training-induced changes on automatism, conduction and myocardial refractoriness are not mediated by parasympathetic postganglionic neurons activity

The purpose of this study is to test the role that parasympathetic postganglionic neurons could play on the adaptive electrophysiological changes produced by physical training on intrinsic myocardial automatism, conduction and refractoriness. Trained rabbits were submitted to a physical training protocol on treadmill during 6 weeks. The electrophysiological study was performed in an isolated heart preparation. The investigated myocardial properties were: (a) sinus automatism, (b) atrioventricular and ventriculoatrial conduction, (c) atrial, conduction system and ventricular refractoriness. The parameters to study the refractoriness were obtained by means of extrastimulus test at four different pacing cycle lengths (10% shorter than spontaneous sinus cycle length, 250, 200 and 150 ms) and (d) mean dominant frequency (DF) of the induced ventricular fibrillation (VF), using a spectral method. The electrophysiological protocol was performed before and during continuous atropine administration (1 μM), in order to block cholinergic receptors. Cholinergic receptor blockade did not modify either the increase in sinus cycle length, atrioventricular conduction and refractoriness (left ventricular and atrioventricular conduction system functional refractory periods) or the decrease of DF of VF. These findings reveal that the myocardial electrophysiological modifications produced by physical training are not mediated by intrinsic cardiac parasympathetic activity.     

改变在体犬右心负荷对其电生理参数的影响

目的：搪塞改变在体犬右心负荷对其电生理参数的影响。方法：改变右房、右室负荷，测定右房，右室舒张期阈值（ＡＤＰ、ＶＤＴ）；右房、右室相对流尖期（ＡＲＲＰ，ＶＲＲＰ）和右房，右室有效不庆期（ＡＥＲＰ，ＶＥＲＰ）。结果：分级（Ａ级和Ｂ级），机械性地部分阻断右房至右室的血流，右房峰值压力（ＰＲＡＰ）升高和有右室峰值压力（ＰＲＶＰ）降低使人ＡＥＲＰ和ＶＲＲＰ延长；但未发现ＡＤＴ，ＶＤＴ有明显变化。亦未出现     

Can local ventricular fibrillation interval predict ventricular refractory period in human hearts?

Assessment of the spatial dispersion of ventricular refractory periods has become an important part of electrophysiological study in both experimental and clinical settings, because inhomogeneity of ventricular refractoriness is associated with an increased risk of life-threatening ventricular arrhythmias. Previous animal studies in dog and sheep have demonstrated that local ventricular fibrillation (VF) intervals measured from the heart surface correlate well with the ventricular effective refractory periods measured from the same ventricular sites. We hypothesise that local VF intervals may also predict the ventricular refractory periods in human hearts, hence, can be used to assess the spatial dispersion of refractoriness and to predict the risk of ventricular arrhythmias.     

维生素C对抗外源性溶血磷脂酰胆碱所致的离体大鼠工作心脏类缺血再灌注损伤作用

目的 :观察维生素C的对抗外源性溶血磷脂酰胆碱(LPC)所致的离体大鼠工作心脏类缺血再灌注损伤作用。方法 :利用麻醉SD大鼠 ,制备离体大鼠工作心脏模型。C组 :用正常K H液连续灌注 35min ;L组 :用含 5 μmolLPC的K H液灌注 5min ,正常K H液再灌注 30min ;V组 :先用含 10 0 μmol维生素C的K H液灌注 5min ,再用含 5μmolLPC的K H液灌注 5min ,用含 15 0 μmol维生素C的K H液再灌注 30min。结果 :与C组相比 ,再灌后L组心功能指标均明显下降 ,室颤发生率提高 ,灌注液中乳酸脱氢酶(LDH)和丙二醛 (MDA)含量明显升高 ,心肌组织中超氧化物歧化酶 (SOD)活力明显降低。L组相比 ,V组心功能指标均明显升高 ,无室颤发生 ,灌注液中LDH和MDA含量明显降低 ,心肌组织中SOD活力变化不明显。结论 :维生素C对LPC所致的心肌类缺血再灌注损伤有明显的对抗作用。     

阿托伐他汀对慢性兔房颤模型心房电重构的影响

目的:通过快速起搏心房3周建立慢性兔房颤模型,探讨阿托伐他汀(ATO)对该模型心房电重构的影响及其可能机制。方法:将24只新西兰大白兔开胸,于左心房植入起搏和测试电极,随机分为3组:模型(model)组和ATO组持续心房起搏3周,分别给予安慰剂和阿托伐他汀2.5 mg·kg~(-1)·d~(-1)灌胃;假手术(sham)组不起搏,不给药。起搏前后用电生理刺激仪检测心率、P波宽度、心房有效不应期(AERP)和房颤诱发率的变化;起搏后采用Western blot检测心房Cav1.2、Kv4.3和髓过氧化物酶(MPO)的蛋白表达水平。结果:Sham组、model组和ATO组分别有0、5和4只兔诱发持续性房颤。起搏3周后,与sham组相比,model组和ATO组兔心率和P波宽度均增加,AERP缩短(P0.05);ATO组与model组相比,AERP增加(P0.05),心率和P波宽度无明显变化。与sham组相比,model组和ATO组兔心房Cav1.2和Kv4.3的蛋白表达水平下降,MPO的蛋白表达水平升高(P0.05);ATO组与model组相比,Cav1.2的表达增加,MPO的表达下降(P0.05),Kv4.3无明显变化。结论:阿托伐他汀能够通过抑制慢性兔房颤模型心房Cav1.2蛋白表达下降和AERP的缩短,抑制心房电重构,其潜在机制可能是阿托伐他汀抑制了心房MPO蛋白的高表达。     

右心室快速起搏致心力衰竭犬的心室电生理特性

目的: 研究右心室快速起搏致充血性心力衰竭(CHF)犬心室电生理特性。方法： 16只犬随机分为正常对照组（n=7）和CHF组（n=9），应用右心室快速起搏（240 pulse·min^-1）4-5周制作CHF犬模型，应用心脏电刺激和单相动作电位（MAP）记录技术测定心室生理指标。结果： （1）CHF组心室有效不应期、心室MAP时程、复极后期及传导时间均延长，分别延长26%（P<0.01）、43%（P<0.01）、318%（P<0.05）和19%（P<0.01）；（2）CHF组心室有效不应期与MAP时程的比值减小13%（P<0.05）；（3）CHF组兴奋恢复时间离散性增加185%（P<0.01）；（4）CHF组室颤阈值降低48%（P<0.01）。结论： CHF异常的心室电生理特性可能是导致恶性心律失常及心脏性猝死发生的基础。     

心脏收缩力调节对慢性心力衰竭兔心室肌电重构的影响

目的:观察心脏收缩力调节(cardiac contractility modulation, CCM)对慢性心力衰竭兔心室肌电重构的影响并探讨其可能的机制。方法:30只新西兰大白兔随机分为3组:假手术组、心衰组(采用升主动脉根部套扎法建立兔慢性心力衰竭模型)和心衰+CCM刺激组(模型制作成功后给予4周的CCM治疗)。电生理记录仪测定QTc和心室有效不应期(ventricular effective refrective period, VERP);采用RT-qPCR和Western blot检测心室肌Kv1.4、Kv4.3和缝隙连接蛋白43 (connexin 43, Cx43)的mRNA和蛋白的表达水平。结果:(1)实验第12周末,心衰兔QTc显著延长(P<0.05);实验第16周末,与心衰组相比,心衰+CCM组经4周CCM刺激后QTc显著缩短(P<0.05)。实验第16周末,与假手术组相比,心衰组、心衰+CCM组VERP显著延长(P<0.05);与心衰组相比,CCM可缩短心衰模型兔的VERP(P<0.05)。(2)与假手术组相比,心衰组心肌组织中Kv1.4、...     

高频刺激左心房引起家兔慢性心房颤动

目的： 探讨以高频率起搏刺激左心房建立家兔慢性心房颤动模型的方法。 方法： 20只家兔随机分为实验组及对照组，对照组为假手术组，植入起搏器但不起搏，实验组10只家兔予开胸植入高频率起搏器(1 000 次/分)刺激左心房30 d，术后定期监测起搏、心房颤动的发生情况、房颤时心室率变化，同时测定起搏前及房颤发生后心房有效不应期（AERP）的变化。 结果： 实验组均完成了实验，术后第7 d，7只（70％）兔发生了房颤，2周时共有8只（80％）发生了房颤并能稳定维持（与对照组比较，P＜0.01），30 d时仍示房颤，其余2只兔至30 d时仍呈起搏心律，对照组则未发生任何心律失常情况。心房颤动时的心室率最初明显增快（P＜0.05），随后有所降低（P＜0.05），但仍高于基础心室率（P＜0.05）。AERP缩短，AERP频率适应不良，与基础状态相比有显著意义。 结论： 长期高频率起搏刺激家兔左心房是建立慢性房颤模型的有效方法。     

Atrial arrhythmogenesis in wild-type and Scn5a+/Δ murine hearts modelling LQT3 syndrome

Long QT(3) (LQT3) syndrome is associated with abnormal repolarisation kinetics, prolonged action potential durations (APD) and QT intervals and may lead to life-threatening ventricular arrhythmias. However, there have been few physiological studies of its effects on atrial electrophysiology. Programmed electrical stimulation and burst pacing induced atrial arrhythmic episodes in 16 out of 16 (16/16) wild-type (WT) and 7/16 genetically modified Scn5a+/Δ (KPQ) Langendorff-perfused murine hearts modelling LQT3 (P < 0.001 for both), and in 14/16 WT and 1/16 KPQ hearts (P < 0.001 for both; Fisher’s exact test), respectively. The arrhythmogenic WT hearts had significantly larger positive critical intervals (CI), given by the difference between atrial effective refractory periods (AERPs) and action potential durations at 90% recovery (APD₉₀), compared to KPQ hearts (8.1 and 3.2 ms, respectively, P < 0.001). Flecainide prevented atrial arrhythmias in all arrhythmogenic WT (P < 0.001) and KPQ hearts (P < 0.05). It prolonged the AERP to a larger extent than it did the APD₉₀ in both WT and KPQ groups, giving negative CIs. Quinidine similarly exerted anti-arrhythmic effects, prolonged AERP over corresponding APD₉₀ in both WT and KPQ groups. These findings, thus, demonstrate, for the first time, inhibitory effects of the KPQ mutation on atrial arrhythmogenesis and its modification by flecainide and quinidine. They attribute these findings to differences in the CI between WT and mutant hearts, in the presence or absence of these drugs. Thus, prolongation of APD₉₀ over AERP gave positive CI values and increased atrial arrhythmogenicity whereas lengthening of AERP over APD₉₀ reduced such CI values and produced the opposite effect.     

Refractory dispersion promotes conduction disturbance and arrhythmias in a Scn5a +/? mouse model

Accentuated right ventricular (RV) gradients in action potential duration (APD) have been implicated in the arrhythmogenicity observed in Brugada syndrome in studies assuming that ventricular effective refractory periods (VERPs) vary in concert with APDs. The present experiments use a genetically modified mouse model to explore spatial heterogeneities in VERP that in turn might affect conduction velocity, thereby causing arrhythmias. Activation latencies, APDs and VERPs recorded during programmed S1S2 protocols were compared in RV and left ventricular (LV) epicardia and endocardia of Langendorff-perfused wild-type (WT) and Scn5a (+/-) hearts. Scn5a (+/-) and WT hearts showed similar patterns of shorter VERPs in RV than LV epicardia, and in epicardia than endocardia. However, Scn5a (+/-) hearts showed longer VERPs, despite shorter APD(90)s, than WT in all regions examined. The pro- and anti-arrhythmic agents flecainide and quinidine increased regional VERPs despite respectively decreasing and increasing the corresponding APD(90)s particularly in Scn5a (+/-) RV epicardia. In contrast, Scn5a (+/-) hearts showed greater VERP gradients between neighbouring regions, particularly RV transmural gradients, than WT (9.1 ± 1.1 vs. 5.7 ± 0.5 ms, p < 0.05, n = 12). Flecainide increased (to 21 ± 0.9 ms, p < 0.05, n = 6) but quinidine decreased (to 4.5 ± 0.5 ms, p < 0.05, n = 6) these gradients, particularly across the Scn5a (+/-) RV. Finally, Scn5a (+/-) hearts showed greater conduction slowing than WT following S2 stimuli, particularly with flecainide administration. Rather than arrhythmogenesis resulting from increased transmural repolarization gradients in an early, phase 2, reentrant excitation mechanism, the present findings implicate RV VERP gradients in potential reentrant mechanisms involving impulse conduction slowed by partial refractoriness.     

阿托伐他汀对快速起搏兔房颤模型心房电重构的影响

 目的: 观察阿托伐他汀(ATO)对快速起搏兔房颤模型心房电重构、心房肌离子通道蛋白及心脏功能的影响,探讨阿托伐他汀防治心房颤动的电生理机制。方法: 30只新西兰大白兔开胸植入心房起搏和测试电极,采用特制动物心脏起搏器快速起搏心房的方法建立兔房颤模型,将其分为对照组、起搏组和药物组。药物组预先给予阿托伐汀钙片2 mg·kg^-1·d^-1灌胃7 d,起搏组和药物组快速起搏心房48 h,期间药物组持续给药处理,分别于0 h、8 h、16 h、24 h、32 h、40 h、48 h测量心房有效不应期,计算心房频率适应性,观察心脏大小及心功能的变化,比较各组心房肌细胞离子通道蛋白CaLα1和Kv4.3的表达差异。结果: 与对照组相比,药物组和起搏组心房有效不应期缩短,频率适应性下降,心房肌细胞离子通道蛋白CaLα1及Kv4.3表达水平降低(P<0.05),其中以起搏组变化最为明显。快速起搏心房48 h后,起搏组和药物组左房较对照组增大(P<0.05),而左心室大小及射血分数起搏前后均无明显差异。结论: 短期快速心房起搏可引起心房有效不应期缩短,导致心房频率适应性不良,阿托伐他汀预处理可有效改善快速起搏诱导的兔心房电重构,而对心脏结构影响不大。进一步研究发现阿托伐他汀可在一定程度上抑制心房肌钾、钙离子通道蛋白水平降低,这可能是其改善电重构的机制之一。     

儿茶酚抑素对慢性心力衰竭大鼠室性心律失常的影响

 目的：探讨儿茶酚抑素(CST)治疗对慢性心力衰竭(CHF)大鼠室性心律失常(VA)的影响。方法：雄性SD大鼠51只，随机分为对照(CTL)组(n=17)和CHF组(n=34)。CHF组给予连续7 d注射异丙肾上腺素(ISO) (5 mg·kg-1·d-1, ip)，CTL组则用生理盐水作为对照 (1 mL·kg-1·d-1, ip)，造模结束2周后，进一步将CHF组再随机分为未治疗组(n=17)和CHF治疗组(CST组)(n=17)。治疗组给予连续3周注射CST(2 nmol·kg-1·d-1, ip)，未治疗组注射0.9%生理盐水(1  mL·kg-1·d-1, ip)。动物完成药物注射后，在整体心脏Langendorff灌流条件下行离体电生理研究，分别记录和测量左室前游离壁(LAF)心外膜单相动作电位(MAP)和心室有效不应期(VERP)；行程控增频电刺激以观察动作电位时程(APD)电交替(ALT)；给予Burst快速电刺激进行VA的诱发。用酶解法分离获得LAF处单个心室肌细胞，采用全细胞膜片钳技术记录L型Ca2+通道电流(ICa-L)。结果：与CTL组相比，未治疗组ICa-L峰电流密度、90%单相动作电位时程(MAPD90)、VERP、诱发APD-ALT最大起搏周长(PCLmax)中位数及VA诱发率均显著增大(均P<0.01)；而CST组MAPD90和VERP均增大(P<0.01)，其它指标差异无统计学意义(均P>0.05)；与未治疗组相比，CST组ICa-L峰电流密度、MAPD90、VERP、诱发APD-ALT的PCLmax中位数(80 ms vs 100 ms)及VA诱发率均减小(均P<0.05)，而VERP/MAPD90增大。结论：CST治疗可减少CHF大鼠VA诱发率，其机制可能与CST抑制CHF大鼠ICa-L有关。     

Regional frequency variation during human ventricular fibrillation

Quantifying the regional frequency variation in ventricular fibrillation (VF) may lead to focal strategies in treating human VF. We hypothesized that during human VF there are quantifiable regional frequency variations in the ventricles and they relate to underlying fixed myocardial substrate. In eight myopathic human hearts, we studied 35 VF episodes. The electrograms during VF were acquired simultaneously from the epicardium and endocardium using 2 electrode arrays each consisting of 112 electrodes. Regional characterization was performed using a ratio parameter derived from the dominant frequency analysis of the electrograms. The findings were related to the anatomical substrate using bipolar voltage maps. The results of the analysis indicate that LV had a larger dominant frequency (DF) span than RV (p=0.0111) while there was no significant difference (p=0.1488) in the DF span between LV freewall (FW) and septum (SE). Correlation of areas of abnormal myocardium with the dominant frequency feature matched only in 50% of the cases indicating that ion channel heterogeneity and time-varying physiological factors may play an important role in maintaining VF.     

Scn3b knockout mice exhibit abnormal sino-atrial and cardiac conduction properties

Aim: In contrast to extensive reports on the roles of Na_v1.5 α-subunits, there have been few studies associating the β-subunits with cardiac arrhythmogenesis. We investigated the sino-atrial and conduction properties in the hearts of Scn3b^−/− mice. Methods: The following properties were compared in the hearts of wild-type (WT) and Scn3b^−/− mice: (1) mRNA expression levels of Scn3b, Scn1b and Scn5a in atrial tissue. (2) Expression of the β₃ protein in isolated cardiac myocytes. (3) Electrocardiographic recordings in intact anaesthetized preparations. (4) Bipolar electrogram recordings from the atria of spontaneously beating and electrically stimulated Langendorff-perfused hearts. Results: Scn3b mRNA was expressed in the atria of WT but not Scn3b^−/− hearts. This was in contrast to similar expression levels of Scn1b and Scn5a mRNA. Immunofluorescence experiments confirmed that the β₃ protein was expressed in WT and absent in Scn3b^−/− cardiac myocytes. Lead I electrocardiograms from Scn3b^−/− mice showed slower heart rates, longer P wave durations and prolonged PR intervals than WT hearts. Spontaneously beating Langendorff-perfused Scn3b^−/− hearts demonstrated both abnormal atrial electrophysiological properties and evidence of partial or complete dissociation of atrial and ventricular activity. Atrial burst pacing protocols induced atrial tachycardia and fibrillation in all Scn3b^−/− but hardly any WT hearts. Scn3b^−/− hearts also demonstrated significantly longer sinus node recovery times than WT hearts. Conclusion: These findings demonstrate, for the first time, that a deficiency in Scn3b results in significant atrial electrophysiological and intracardiac conduction abnormalities, complementing the changes in ventricular electrophysiology reported on an earlier occasion.     

拟交感效应对快速起搏离体心脏心房缝隙连接蛋白43重构的影响

目的:通过建立离体拟交感心房颤动模型,探讨缝隙连接蛋白43(Cx43)水平的变化。方法:15只杂种犬随机分为3组(每组5只):对照组(control组)、快速心房起搏组(RAP组)和异丙肾上腺素灌流+快速心房起搏组(ISO+RAP组)。经胸骨正中切开术,快速取出心脏,建立心脏Langendorff离体灌流模型。各组分别检测心房有效不应期(AERP)及房颤诱发率,免疫组化检测酪氨酸羟化酶(TH)在细胞内的表达,Western blot检测Cx43和磷酸化Cx43的蛋白含量,免疫荧光检测Cx43在心肌组织的变化,TUNEL法检测心肌细胞凋亡,荧光比色法检测线粒体活性氧簇(ROS)的生成量。结果:与control组比较,RAP组的AERP无明显变化,且仅出现电紊乱,ISO+RAP组的AERP明显缩短(P0.05),并可成功诱发房颤。与control组比较,RAP组和ISO+RAP组的TH表达量、细胞凋亡指数和线粒体ROS生成量均逐渐增多(P0.05),Cx43蛋白表达量和磷酸化水平逐渐减少(P0.05)。免疫荧光显示,与control组相比,RAP组的Cx43荧光强度降低,且呈明显侧链化,ISO+RAP组则呈点状散在分布。结论:交感神经可能通过氧化应激效应,引起Cx43的重构与下调,从而介导心房颤动的发生。     

非接触标测和频谱分析迷走神经介导的心房颤动

目的： 对在体犬迷走神经介导的心房颤动（房颤）进行非接触标测和频谱分析，以探讨其发生和维持机制。方法: 测定8只犬基础情况及双侧迷走神经刺激时心房有效不应期及其离散度，非接触标测和频谱分析房颤时左、右房的电活动。结果: 迷走神经刺激与基础情况相比，左、右心房有效不应期缩短，但有效不应期离散度增大仅见于左房。迷走神经刺激时房颤易诱发和维持，房颤显示反复有序的激动经优先传导路径传播仅见于左房；频谱分析显示左房的主导频谱高于右房［（12.5±1.5)Hz vs (9.3 ±1.2) Hz，P<0.05］。停止迷走神经刺激，左、右房房颤频谱降低［（9.2±0.5)Hz vs (8.5±0.6)Hz， P>0.05］，房颤自发终止。结论: 左、右房电生理特性改变、激动模式差异以及频谱梯度提示迷走神经介导的房颤发生和维持依赖于左房。     

Ruthenium red-induced transition from ventricular fibrillation to tachycardia in isolated rat hearts:: possible involvement of changes in mitochondrial calcium uptake

INTRODUCTION: Ventricular tachycardia (VT) is considered to be the most common precursor of ventricular fibrillation (VF) and sudden cardiac death. However, the mechanisms underlying the transition from VT to VF remain unclear despite more than a century of study. Here, we investigated whether perfusion of the heart with blockers of mitochondrial Ca(2+) uniporter changed the macrodynamics of the heart between VT and VF. METHODS: The experiments were performed using Langendorff perfused isolated rat hearts in which left ventricular pressure (LVP) and left ventricular cardiomyogram (LVCMG) were measured. Sustained VT or VF was induced by burst pacing of the left ventricular muscles. RESULTS: During pacing-induced sustained VF, perfusion of the heart with ruthenium red (RR) or Ru 360, blockers of mitochondrial Ca(2+) uniporter, resulted in the reversible conversion of VF to VT. In contrast, during pacing-induced sustained VT, perfusion of the heart with spermine, an activator of mitochondrial Ca(2+) uptake, resulted in the reversible conversion of VT to VF, and the effect was antagonized by cotreatment with RR. In addition, RR-induced conversion of VF to VT was antagonized by cotreatment with S(-)-Bay K8644 (Bay K), an activator of L-type Ca(2+) channels, suggesting that the inactivation of L-type Ca(2+) channels was responsible for the RR-induced effect on the macrodynamics of hearts. In fact, perfusion with verapamil, an antagonist of L-type Ca(2+) channels, during pacing-induced sustained VF, resulted in the conversion of VF to VT. CONCLUSION: This study demonstrated that perfusion of isolated rat hearts with blockers of Ca(2+) uptake by mitochondria resulted in the reversible conversion of pacing-induced sustained VF to VT, suggesting that changes in mitochondrial Ca(2+) uptake were possibly involved in the transition between VT and VF.     

链霉素对兔左心室后负荷增加所致电生理变化的影响

目的:探讨左心室后负荷增加引起的心脏电生理变化及链霉素和维拉帕米对其的影响。方法:采用部分夹闭家兔升主动脉根部以增加左室后负荷的在体心脏模型,观察后负荷增加前后心肌相对不应期(RRP)、有效不应期(ERP)、单相动作电位时程(MAPD₉₀)和室颤阈(VFT)的变化,并比较了链霉素和维拉帕米对这些电生理参数变化的影响。结果:后负荷上升引起RRP、ERP和MAPD₉₀缩短,VFT下降(P<0.01);链霉素可有效抑制后负荷增加引起的心脏电生理变化;而维拉帕米除可提高VFT外(P<0.01),对后负荷增加引起RRP、ERP和MAPD90的缩短没有明显影响(P＞0.05)。结论:结果提示牵张激活性离子通道的活化可能参与后负荷增加引起的心脏电生理变化过程,且链霉素通过抑制这种离子通道的活化而发挥作用。     

高频起搏犬房颤模型心房重塑及窦房结和房室结功能的变化

 目的:持续高频起搏犬左心房,观察房颤(AF)发生率、心房重塑以及窦房结、房室结传导功能。方法: 健康比格犬15只随机分为起搏组(P组,n=9)和对照组(N组,n=6)。2组均在左心房心外膜缝合固定一起搏电极,P组以400 min-1的频率起搏,N组不起搏。采用程序起搏技术测定电生理参数。结果: (1) 4周后P组阵发性AF和持续性AF的诱发率与N组比较差异均有统计学意义（分别P<0.05,P<0.01）,P组第2周2只犬自发AF,第4周AF诱发率达100%,且持续性AF的发生率高。 (2) P组4周后心房有效不应期(AERP)在不同基本起搏周期(250 ms、300 ms和350 ms)时均较N组缩短 (P<0.05);房室结文氏点(AVN-Wen) 较N组有意义延长［(294.44±26.03)min-1 vs (328.33±24.01)min-1, P<0.05］;房室结有效不应期(AVERP)在不同起搏周期均明显延长 (P<0.01)。(3) 与N组比较,P组4周后窦房结恢复时间（SNRT）和校正恢复时间（cSNRT）均延长（P<0.01）;P波时限2组比较差异没有统计学意义(P>0.05)。(4) P组2周后心脏超声与N组比较显示左心房前后、上下、左右径都有明显增大(P<0.01),右心房上下增大(P<0.05)。结论: 持续４周心房高频起搏后房颤发生率高,心房肌、窦房结和房室结电生理发生特征性的相应改变,左、右心房不同程度扩大,提示电重塑、结构重塑与房颤的发生关系密切。     

组织工程化心肌片层移植心肌梗死大鼠的心功能及电生理变化

背景：组织工程化心肌组织在组成结构上类似于心脏组织的三维电偶联网络和肌肉横纹,而且具有心肌组织样收缩功能,为病损心肌提供了修复的可能性。 目的：观察心肌细胞/胶原复合体移植后心肌梗死大鼠心室肌的心功能及电生理变化。 方法：将成年SD大鼠分为假手术组、模型组、移植组,后2组制作心肌梗死动物模型,假手术组仅开胸,不结扎冠状动脉。移植组移植心肌细胞与胶原材料复合组织,其他2组不进行移植。 结果与结论：①左室心功能：与假手术组相比,模型组左室舒张末期内径、左室收缩末期内径均显著增大(P < 0.01),左室射血分数和左室短轴缩短率显著降低(P < 0.01);移植组左室舒张末期内径、左室收缩末期内径、左室射血分数和左室短轴缩短率均未见明显增大或降低(P > 0.01)。②左室有效不应期变化：与假手术组相比,模型组梗死周边区有效不应期显著缩短(P < 0.01);移植组梗死周边区有效不应期较模型组延长,差异有显著性意义(P < 0.01)。③Cx43免疫荧光结果：假手术组、模型组和移植组大鼠缝隙连接蛋白43阳性表达依次呈现阳性,弱阳性,弱阳性。但移植组缝隙连接蛋白43阳性表达高于模型组。结果可见移植的心肌细胞/胶原复合体在组织和结构上形成电偶联网络和收缩偶联,能改善心肌梗死大鼠心室肌的收缩功能及电生理特性。