Experimental Study of the Effect of Autonomic Nervous System on the Transmural Dispersion of Ventricular Repolarization under Acute Myocardial Ischemia in Vivo

The electrophysiologic heterogeneity of the ven-tricular myocardium is an important factor of devel-oping ventricular arrhythmia.Under the pathologiccondition,thedistribution and thefunction of the au-tonomic nerves,especially the sympathetic nerve,can produce the heterogeneity in the myocardium,which can accelerate the electrophysiologic hetero-geneity of the ventricular myocardium.Acute my-ocardial ischemia can induce the dysfunction of theautonomic nerve endings,resulting in the hetero-gene…     

Effect of autonomic nervous system on the transmural dispersion of ventricular repolarization in intact canine

Therecentstudieshavefoundasub populationofcells ,namedmidmyocardiumcells(Mcell) ,withuniqueelectrophysiological propertiesinthedeepsubepicardiumoftheventricleofhuman ,canineandotheranimals .TheresearcherssuggestedthattheMcellsnotonlyformthecellularbasisof…     

Effect of Autonomic Nervous System on the Transmurai Dispersion of Ventricular Repolarization in Intact Canine

Summary: The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization in intact canine was investigated. By using the monophasic action potential (MAP) recording technique, monophasic action potentials (MAPs) of the epicardium (Epi), midmyocardium (Mid)and endocardium (Endo) were recorded simultaneously by specially designed plunge-needle electrodes at the left ventricular free wall in 12 open-chest dogs. MAPD90 and transmural dispersion of repolarization among three myocardial layers as well as the incidence of the EAD before autonomic nervous stimulation and during autonomic nervous stimulation were compared. The results showed that the MAPD90 of Epi, Mid and Endo before autonomic nervous stimulation were 278±11 ms,316± 16 ms and 270± 12 ms respectively, the MAPD90of Mid was significantly longer than that of Epi or Endo (P＜0.01). MAPD90 of Epi, Mid and Endo were shortened by 19±4 ms, 45±6 ms,18± 3 ms respectively during sympathetic stimulation. Compared with that of the control, the transmural dispersion of repolarization during sympathetic stimulation was shortened from 44 ± 4 ms to 15±3 ms (P＜0. 01), but early afterdepolarizations were elicited in the Mid of 5 dogs (41 0%)during sympathetic stimulation. Parasympathetic stimulation did not significantly affect the MAPD90 in the three layers. It is concluded that there is the transmural dispersion of ventricular repolarization in intact canine. Sympathetic stimulation can reduce transmural dispersion of repolarization, but it can produce early afterdepolarizations in the Mid. Parasympathetic stimulation does not significantly affect the transmural dispersion of ventricular repolarization.     

Effect of Lidocaine and Amiodarone on Transmural Heterogeneity of Ventricular Repolarization in Isolated Rabbit Hearts Model of Sustained Global Ischemia

Someresultsofmeta analysesofrandomizedcontroltrialsonmyocardialinfarctionfoundthatlidocaineandamiodaronecanbeusedforthetreat mentofventriculartachyarrhythmias,butlido cainedonotreducemortalityinpatientswithven triculararrhythmiasaftermyocardialinfarctionwhileamiodaronecan[1,2].Themechanismisnotfullyunderstood.Inrecentyears,discoveryoftheMcells,andthreelayersmyocardiumtheorybeendrawed,thatmostelectrophysiologicalphenomenahadgotnewexplains[3,4].Thisexperimentthemonophasicactionpotentials(MAPs)…     

Changes of monophasic action potential duration and effective refractory period of three layers myocardium of canine during acute ischemia in Vivo

Summary The effect of acute ischemia on the electrophysiological characteristics of the three layers myocardium of caninein vivo was investigated. Twelve canines were divided into two groups randomly: acute ischemia (AI) group and sham operation (SO) group. By using the monophasic action potential (MAP) technique, MAP and effective refractory period (ERP) of the three layers myocardium were measured by specially designed plunge needle electrodes and the transmural dispersion of repolarization (TDR) and transmural dispersion of ERP (TDE) were analyzed. The results showed that in the AI group, MAP duration (MAPD) was shortened from 201.67±21.42 ms to 169.50±13.81 ms (P<0.05), but ERP prolonged to varying degrees and TDE increased during ischemia. In the SO group, MAPD and ERP did not change almost. Among of the three layers myocardium of canine, MAPD was coincident in two groups. It was concluded that during acute ischemia, MAPD was shortened sharply, but there was no significant difference among of the three layers myocardium. The prolonged ERP was concomitant with increased TDE during acute ischemia, which may play an important role in the occurrence of arrhythmias induced by acute ischemia. These findings may have important implications in arrhythmogenesis. ZHANG Fanzhi, male, born in 1973, M. D., Ph. D.     

Effect of Lidocaine and Amiodarone on Transmural Heterogeneityricular Repolarization in Isolated Rabbit Hearts Model of Sustained Global Ischemia

To study the effect of of lidocaine and amiodarone on the transmural heterogeneity of ventricular repolarization in isolated rabbit hearts model of sustained global ischemia and to explore the mechanisms underlying the antiarrhythmic activity of lidocaine and amiodarone, rabbits were randomly divided into 4 groups: control group, ischemia group, lidocaine group and amiodarone group. By the monophasic action potential (MAP) recording technique, MAPs of recorded across the left ventricular free wall in rabbit hearts perfused transmural dispersion of repolarization (TDR) and arrhythmic induced by ischemia. Our results showed that TDR of three myocardial layers in ischemia group were significantly lengthened after ischemia. TDR was increased from 17.5±3.9 ms to 31.2±4.6 ms at the time that concided with the onset of sustained ventricle arrhythmic. Amiodarone could decrease TDR, but lidocaine could increase TDR at initial ischemia, and no significant difference was found at other ischemia time points. 5 cases had ventriclar arrhythmia in ischemia group (62.5 %), but no case in lidocaine group (P<0.01) and only 1 case in amiodarone group had ventrilar arrhythmia (P< 0.01). No significant difference was found between amiodarone group and lidocaine group. It is concluded that TDR of of three myocardial layers increases significantly at ischemia and it is closely associated with development of ventricular arrhythmia, and amiodarone could decrease TDR, but lidocaine could increase TDR at initial ischemia and has no effects at other ischemia time points.     

药物致尖端扭转型室性心动过速的发生机制

目的探讨药物致尖端扭转型室性心动过速（Tdp）的发生机制。方法建立冠状动脉灌注的犬左室心肌楔形组织块模型,
同步记录左心室内膜、中层、外膜心肌细胞的动作电位及跨壁心电图,观察不同浓度D-Sotalol对动作电位时间（APD）、QT间期、
跨壁复极离散度（TDR）、早期后除极（EAD）及Tdp发生的影响。结果浓度为0~100 μmol/L的D-Sotalol呈剂量依赖性地延长
各层细胞APD,尤以中层细胞最为显著（P<0.05）,因而增加TDR;D-Sotalol在中层细胞可诱发EAD,触发室性早博并形成跨壁
折返导致Tdp。结论D-Sotalol在中层细胞诱发EAD、R on T室性早博是其致Tdp的始动因子,在TDR增加的基础上形成跨室
壁折返是Tdp得以维持的关键。
     

扩张型心肌病家兔左室壁复极异质性的改变及意义

目的：观察离体心脏左心室三层心肌的单相动作电位的改变，以探讨扩张型心肌病易发心室颤动与三层心肌跨室壁复极不均一性的关系。方法：用阿霉素制作扩张型心肌病家兔模型，测定其室颤阈值（VFT）以及心外膜、中层心肌和心内膜心肌细胞的单相动作电位复极90％时程（APD90）、跨室壁复极离散度（TDR）。结果：扩张型心肌病VFT明显降低（P＜0．001），三层心肌细胞APD90均明显延长（P＜0．001），中层心肌细胞较心外膜、心内膜下心肌细胞延长更为显著（P＜0．05）；扩张型心肌病跨室壁复极离散度增加（P＜0．01）。结论：中层心肌细胞APD90明显延长、跨室壁复极离散度增加、三层心肌复极不均一性增加可能是扩张型心肌病容易发生心室颤动的重要原因。     

犬在体心肌跨室壁复极不均一性的实验研究

目的 :探讨犬在体心肌是否存在跨室壁复极不均一性。方法 :40 %的甲醛溶液 0 1～ 0 3ml注入房室结 ,制备完全性房室传导阻滞模型 ,心室起搏控制心室率。应用单相动作电位记录技术 ,同步记录犬在体心外膜 (epi cardium ,Epi)、中层 (midmyocardium ,Mid)及心内膜 (endocardium ,Endo)心肌单相动作电位 (MAP) ,测量单相动作电位时程 (MAPD)并比较其差异。结果 :在心动周期 (cyclelength ,CL) 30 0ms时 ,Epi、Mid、Endo的MAPD90 分别为 2 0 8 6 7± 44 37ms、2 0 9 17± 38 6 2ms、2 0 3 5 0± 33 84ms(n =10 ) ,在体三层心肌单相动作电位时程无明显差异 ,CL增加至2 0 0 0ms时 ,三层心肌MAPD呈慢频率依赖性延长 ,Epi、Mid、Endo的MAPD90 分别为 32 9 90± 31 90ms、36 9 90±35 0 9ms、317 2 0± 40 2 7ms ,其中Mid的MAPD90 延长最为显著 ,与Epi及Endo相比 ,差异有显著性意义 (P <0 0 5 )。结论 :犬在体心肌存在明显慢频率依赖性的跨室壁复极不均一性     

Experimental study on the mechanism of sex difference in the risk of torsade de pointes

Torsadedepointes (TdP )isaformofpolymorphicventriculartachycardia (VT)accompaniedbyaprolongedQTinterval FemalesareathigherriskofdevelopingTdP ,especiallyinresponsetodrugsordiseasesthatcanprolongtheQTinterval 1 3　Thequestionofwhyfemalesareathigherriskhasarousedgreatinterest ExperimentsonthistopichavefocusedontheQTintervalaswomennaturallyhavealongerQTintervalthanmen 4 　Buttheresultsofpastexperimentshavebeeninconsistent,5,6 　andthemechanismsoffemalepredominanceinTdPremainunclear Itiskno…     

伊文思兰对兔左室心肌灌注范围显示效果及跨膜动作电位的影响

目的　探讨伊文思兰对于经冠脉灌注的兔左室心肌组织块灌注范围显示效果及跨膜动作电位的影响。方法　制做兔左心室游离壁楔形组织块 ,经回旋支持续灌注台式液。采用浮置的玻璃微电极同步记录内、中、外层心肌细胞跨膜动作电位并记录跨壁心电图。分析伊文思兰灌注前、灌注 30 min后组织块显色情况及不同频率刺激下内、中、外层跨膜动作电位时程和跨壁复极离散度的变化。结果　伊文思兰可清晰显示灌注范围 ,且 30 m in后颜色仍保持不变 ;在 5 0 0～ 4 0 0 0 ms刺激作用下 ,伊文思兰灌注前与灌注 30 m in后动作电位时程、跨壁复极离散度无显著变化 (P>0 .0 5 ) ,灌注过程中组织块无室性心律失常发生。结论　伊文思兰可以作为组织块灌注范围的显示剂     

Changes of Monophasic Action Potential Duration and Effective Refractory Period of Three Layers Myocardium of Canine during Acute Ischemia in Vivo

Ventricular tachyarrhythmias are readily gen-erated in acute ischemia/infarction.The majorityof serious ventricular arrhythmias during ischemiais caused by reentry and occurs withinthe first mi-nutes of onset[1].Moreover,a growing body of ev-idence suggests that heterogeneity of electrophysi-ological characteristics is an i mportant property ofthe ventricular myocardium[2,3].I mportantly,asubpopulation of cells,called midmyocardial cells(Mcells),have been described in the ventricularwall of th…     

普萘洛尔治疗长QT综合征的电生理机制探讨

目的：观察普萘洛尔对家兔跨左室壁不同部位心肌细胞电生理特性的影响，探讨普萘罗尔治疗长QT综合征（LQTS）的电生理机制。方法：采用标准玻璃微电极记录技术，记录心外膜心肌（epicardium，Epi）、中层心肌（mid—myocardium，Mid）和心内膜心肌（endocardium,Endo）的跨膜动作电位（transmembrance action potential，TAP）。用基础周长（basic cycle length，BCL）为2000m刺激心肌标本，观察不同浓度的普萘洛尔对三种心肌TAP的影响。结果：1．普萘洛尔浓度依赖性缩短d—sotalol灌流的三层心肌的APD90，与Epi和Endo相比，Mid的APD90缩短更明显，使TDR降低，且随着剂量的增加这种作用更为显著。2．普萘洛尔浓度依赖性地抑制d—sotalol诱导的早期后除极（Early afterdepolarization，EAD）。结论：普萘洛尔降低三层心肌间的复极离散度和抑制早期后除极是普萘洛尔治疗LQTS的电生理机制。     

Effects of Potassium Aspartate and Magnesium on Ventricular Arrhythmia in Ischemia-reperfusion Rabbit Heart

The aim of this study was to determine if the potassium aspartate and magnesium (PAM) prevent reperfusion-induced ventricular arrhythmias (RIVA) in ischemia-reperfusion (IR) rabbit heart. Thirty rabbits were randomly divided into control, ischemia and PAM groups. Arterially-perfused rabbit left ventricular preparations were made, and transmural ECG as well as action potentials from both endocardium and epicardium were simultaneously recorded in the whole process of all experiments. In control group rabbit ventricular wedge preparations were continuously perfused with Tyrode's solution, and in ischemia group and PAM groups the perfusion of Tyrode's solution was stopped for 30 min. Then the ischemia group was reperfused with Tyrode's solution and the PAM group with Tyrode's solution containing 2.42 mg/L PAM, respectively. ECG, QT interval, transmural repolarization dispersion (TDR) and action potentials from epicardium and endocardium were simultaneously recorded, and the RIVA of the wedge preparation was observed. Compared with control group, TDR and incidence of RIVA were significantly increased in ischemia group (P<0.05). The incidence of RIVA in control, ischemia and PAM group was 0/10, 9/10 and 1/10, respectively. Compared with ischemia group, TDR and incidence of RIVA were significantly reduced in PAM group (P<0.05). Potassium aspartate and magnesium significantly reduce TDR and prevent ventricular arrhythmia in ischemic rabbit heart.     

雷米普利对兔心肌梗死后心室肌电生理的影响

目的:探讨血管紧张素转化酶抑制剂雷米普利对兔心肌梗死后室性心律失常发生的影响及其可能机制.方法:24只家兔随机分为假手术组(SHAM)、心肌梗死组(MI)和雷米普利组(RAM).3组均在无菌条件下开胸,其中心肌梗死组和雷米普利组分别结扎左冠状动脉前降支.雷米普利组术后第2天给予雷米普利[1 mg/(kg·d)],3组共...     

不同血钾水平时索他洛尔对在体跨室壁心肌复极不均一性的影响

为了观察正常血钾和低血钾时索他洛尔对在体跨室壁心肌复极不均一性的影响,探讨索他洛尔致室性心律失常的机制。24只兔随机分为两组,正常血钾组（12只）和低血钾组（12只）,分别静注索他洛尔1.0mg/kg,3.0mg/kg;同步记录兔左室心外膜心肌(Epi)、中层心肌(Mid)和心内膜心肌(Endo)的单相动作电位（MAP）,研究发现低钾时与血钾正常时相比,索他洛尔增加跨室壁心肌复极离散度（TDR）的作用更明显;更易引起Mid发生早期后除极（EAD）;低血钾组尖端扭转性室速（TdP）的发生率亦更高。     

QT离散度与急性心肌梗塞预后的关系

目的:探讨急性心肌梗塞(AMI)病人QT离散度(QTd)的变化与AMI病人预后的关系。方法:192例AMI病人分为存活组171例、死亡组21例,另有正常对照组25例。测定AMI病人和正常人体表12导联心电图的QTd或jT离散度(jTd)的变化。结果:192例AMI病人QTd与jTd分别为61.92±15.2ms,45.86±16.22ms,正常对照组25例QTd与jTd分别为20.32±8.14ms、18.24±8.12ms,两组相比P<0.001。存活组入院时QTd与jTd分别为60.96±12.24ms、45.22±10.24ms,出院时分别为39.26±10.42ms、32.14±12.24ms,入院与出院相比P<0.01。死亡组21例QTd与jTd分别为70.24±15.38ms、66.42±14.24ms,与存活组相比P<0.05。结论:AMI病人 QTd明显增加,QTd的测定对AMI病人预后的估价具有一定的预测性。     

充血性心力衰竭跨室壁复极不均一性的改变

目的研究充血性心力衰竭模型左心室三层心肌之间单相动作电位的改变。以探讨充血性心力衰竭易发心室颤动的基础电生理机制。方法用阿霉素制作充血性心力衰竭家兔模型，测定其室颤阈值（VFT）以及心外膜、中层心肌和心内膜心肌细胞的单相动作电位复极90％时程（APD90）、跨室壁复极离散度（TDR）。结果充血性心力衰竭VFT明显降低，三层心肌细胞APD90均明显延长，但中层心肌细胞较心外膜、心内膜下心肌细胞延长更为显著；充血性心力衰竭跨室壁TDR增加。结论中层心肌细胞APD90明显延长、跨室壁TDR增加可能是充血性心力衰竭容易发生心室颤动的重要原因。     

胺碘酮对左室肥厚家兔跨室壁Cx43异质性的影响

目的：观察胺碘酮片剂对左室肥厚(LVH)家兔三层心肌间Cx43表达的差异,探讨LVH恶性室性心律失常(MVA)的机制及处理措施。方法将20只家兔按随机数字法分成胺碘酮治疗组和LVH对照组,每组各10只。两组家兔均采用传统的腹主动脉缩窄术后继续喂养8周以制备LVH模型。治疗组手术后给予经口喂服盐酸胺碘酮片,每日50 mg/kg,连续4周,然后继续喂养4周并进行实验;对照组喂养生理盐水8周后进行实验。分别检测两组家兔心外膜下、中层心肌和心内膜下心肌细胞的单相动作电位复极90%时程(APD90)、跨室壁复极离散度(TDR)以及左心室三层心肌Cx43蛋白表达的差异。结果(1)治疗组家兔心内、外膜下、中层心肌的APD90分别为(275.30±11.42) ms、(251.50±10.98) ms和(295.40±12.41) ms,均较LVH对照组的(236.30±16.51) ms、(217.69±14.25) ms和(265.12±20.01) ms显著延长,差异具有显著统计学意义(P<0.01),但是治疗组的TDR为(38.96±10.91),明显小于对照组的(48.56±11.23),差异有统计学意义(P<0.05)。(2)治疗组家兔三层心肌的Cx43蛋白表达分别为(0.60±0.07)、(0.48±0.05)和(0.57±0.06),均较对照组的(0.53±0.04)、(0.31±0.06)和(0.48±0.04)明显提高(P<0.05),但以中层心肌的增加更为明显,从而缩小了三层心肌间Cx43蛋白表达的差异,△Cx43减少[(0.14±0.06) vs (0.23±0.08),P<0.01]。结论胺碘酮能改善左室肥厚的跨室壁Cx43表达异质性,缩小左心室心肌跨室壁复极不均一性,这可能是其减少MVA发作的生理机制。     

心肌缺血时复极和传导交替是T波电交替的电生理机制

目的:探讨缺血性T波电交替(TWA)的电生理学机制.方法:在体实验组家兔10只,开胸后结扎左冠状动脉前降支(LAD),造成心肌缺血模型,在结扎LAD前、结扎后60 min重复观测缺血区域心室壁内膜下层、中层和外膜下层的单相动作电位时程(MAPD)、有效不应期(ERP),快速心室刺激诱发TWA.离体实验组家兔10只,快速开胸取出心脏后作Langendorff灌流,先用正常Tyrode's液灌流30 min再用模拟缺血液灌流.在Tyrode's液灌流20 min后、模拟缺血液灌流60 min后重复观测模拟肢体导联心电图,以及左心室前壁、侧壁、右心室和心尖部心外膜的MAPD、ERP,快速心室刺激诱发TWA.结果:缺血后各位点MAPD的频率适应性降低,MAPD90和ERP缩短.与生理状态相比,心肌细胞复极梯度发生了明显重排.20个在体和离体心脏在缺血后全部可用快速心室刺激诱发TWA,诱发TWA的心动周期(CL)窗口在130-170ms之间,CL=140,150 ms时可稳定地诱发TWA.TWA时伴有单相动作电位复极和传导的交替.离体心外膜增频刺激时,CL=170 ms开始出现TWA,随后的减频刺激至CL=200 ms时TWA消失,即TWA的滞后现象.结论:心肌细胞复极不均一可能是引起心电图T波的原因之一.心肌缺血使心脏正常的复极梯度发生改变,在快速心室刺激时易于发生动作电位复极和传导的交替,在体表心电图上表现为TWA.