粉防己碱抗氯化铯诱发家兔在体心脏早后除极及心律失常的作用

目的 :研究粉防己碱 (Tet)抗氯化铯 (CsCl)诱发触发活动及触发性心律失常作用。方法 :14只家兔分对照组和Tet组 ,Tet组给予Tet 0 5mg kg min共 10min ,对照组给予生理盐水 ,然后给予CsCl1 5mmol kg静注 ,给药前后记录心电图和右室心内膜MAP。结果 :Tet组和对照组均诱发EAD ,但Tet组EAD幅度低于对照组 ,室性心律失常发生率低于对照组。结论 :Tet有抗CsCl诱发EAD及室性心律失常作用。其机制可能是Tet抑制慢钙通道 ,减少内向电流。

氯沙坦对犬缺血再灌注心肌损伤的保护作用

目的探讨氯沙坦对犬在体心肌缺血再灌注时心肌损伤的保护作用。方法16只健康家犬,分为2组:(1)对照组(n=8),阻断左前降支主干30min后恢复前降支血流30min。应用单相动作电位记录技术,同步记录犬在体心肌再灌注时单相动作电位及体表心电图;(2)氯沙坦组(n=8):氯沙坦5mg/(kg·d)经胃管灌入,持续2周后开胸,缺血再灌注方法及观察指标同对照组。结果再灌注30min内,对照组8只犬中有5只出现了早期后除极(EAD)和再灌注室性心律失常,再灌注心律失常发生率为62.5%;氯沙坦组3只犬出现EAD和再灌注室性心律失常(37.5%,P<0.05),氯沙坦组EAD和心律失常发生率较对照组明显减小(P<0.01)。结论氯沙坦可抑制再灌注时EAD的发生,可能因此而减少再灌注心律失常的发生。

离体LQT2兔心脏模型的研制

目的室性心律失常是临床常见急诊,长QT综合征(LQTS)所致的尖端扭转型室性心动过速(TdP)是室性心律失常的一种类型。为进一步研究长QT综合征,特制作离体LQT2兔心脏模型。方法新西兰兔共12只,取出心脏,立即行逆行主动脉灌注,然后用有齿镊钳夹房室结造成Ⅲ度房室传导阻滞,分别用1000ms刺激周长(CLs)起搏至少100个心动周期,体表心电图提示无ST-T明显压低或抬高,给予低钾低镁台氏液灌流5min,观察EAD及心律失常情况。然后用加有右旋索他洛尔(d-Sotalol)100μmol/L浓度的台氏液逆行Langendorff灌流30min后再分别用上述刺激周期进行刺激,观察:①90%动作电位时程(APD90);②90%复极时间(RT90);③跨室壁复极离散度(TDR);④早期后去极化(EAD)及尖端扭转型室性心动过速的发生率;⑤平均QT间期等的变化。结果12只新西兰离体Langendorff灌流兔心脏,在心动过缓及高浓度d-Sotalol(100μmol/L)存在时,动作电位时程明显延长,TDR明显增加(P<0.001),并诱发出EAD(11/12,91.67%),但TdP发生率低(3/12,25%),在附加的低钾低镁台氏液灌流时,TdP发生率高(10/12,83.33%)。结论d-sotalol可在Langendroff灌流离体新西兰兔心脏上成功制备LQT2模型。

间歇依赖性长QT间期综合征伴扭转型室性心动过速的电生理探讨

长ＱＴ间期伴扭转型室性心动过速（ＴｄＰ）是临床上常见的严重心律失常。ＴｄＰ的发生机制已有研究，表明可能与触发机制有关。本文对３例不同病因的长ＱＴ间期综合征（ＬＯＴＳ）伴ＴｄＰ的电生理和心内膜单相动作电位记录进行了研究。观察到如下特点：①心室刺激（程序或递增刺激）结合异丙肾上腺素静脉注射均不能诱发室性心律失常；②全部患者心电图上均能记录到巨大Ｕ波；③２例患者，在右心室内膜单相动作电位复极化［３］相期记录到一个驼峰形波，即为后去极化（ＥＡＤ），该驼峰形波与体表心电图上巨大Ｕ波同步发生。本研究表明ＥＡＤ在ＬＱＴＳ伴ＴｄＰ的发生中可能起重要作用。

硫酸镁对早期后去极和室性心律失常的抑制作用

镁治疗室性心律失常的机制还不清楚，本实验以Ｆｒａｎｚ心内膜接触电极研究镁对氯化铯引起的大室性心律失常作用。结果表明，氯化铯可引起早期后去极（ＥＡＤ）和室性心律失常，镁治疗组的ＥＡＤ幅度明显低于对照组（９．２±２．２％ＭＡＰ，２０．３±２．４％ＭＡＰ，Ｐ＜０．０１）。室性心律失常的发生率由对照组的１００％降为３７．５％（Ｐ＜０．０１）。硫酸镁可缩短延长了的ＱＴｃ间期。本文提示，硫酸镁对ＥＡＤ的抑制作用可能是抗心律失常的机制所在。

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

Summary: The effect of the autonomic nerves on the transmural dispersion of ventricular repolarization (TDR) under acute myocardial ischemia in intact canine was investigated. Using the monophasic action potential (MAP) recording technique, 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 under acute myocardial ischemia in 12 open-chest dogs. MAPD 90 and TDR among three myocardial layers as well as the incidence of the early afterdepolarization (EAD) before autonomic nervous stimulation and during autonomic nervous stimulation were compared. It was found that 10 min after acute myocardial ischemia, TDR was increased from 55±8 ms to 86±15 ms during sympathetic stimulation (P<0.01). The TDR (53±9 ms) during parasympathetic stimulation was not significantly different from that of the control (55±8 ms) (P>0.05). The EAD was elicited in the Mid of 2 dogs (16 %) 10 min after acute myocardial ischemia, but the EAD were elicited in the Mid of 7 dogs (58 %) during sympathetic stimulation (P<0.01). It was concluded that: (1) Sympathetic stimulation can increase the transmural dispersion of repolari-zation and induce early afterdepolarizations in the Mid under acute myocardial ischemia, which provide the opportunity for the ventricular arrhythmia developing; (2) Parasympathetic stimulation has no significant effect on the transmural dispersion of repolarization under myocardial ischemia.

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

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. MAPD 90 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 MAPD 90 of Epi, Mid and Endo before autonomic nervous stimulation were 278±11 ms, 316±16 ms and 270±12 ms respectively, the MAPD 90 of Mid was significantly longer than that of Epi or Endo ( P <0.01). MAPD 90 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 %) during sympathetic stimulation. Parasympathetic stimulation did not significantly affect the MAPD 90 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.

犬在体心肌再灌注时早期后除极起源的实验研究

目的 观察再灌注时犬在体心肌早期后除极 (EAD)的起源。方法 12只健康犬 ,阻断左前降支主干 30 min后恢复前降支血流制备再灌注模型。应用单相动作电位记录技术 ,同步记录犬在体心肌再灌注时心外膜、中层和心内膜心肌 MAP及体表心电图 ,分析其相关参数的变化。结果 再灌注 30 m in内 ,12只犬中有 9只出现了 EAD(75 % ) ,Epi、Mid及 Endo的 EAD振幅 (EADA)分别为 3.44± 1.6 3m V、5 .49± 1.2 4m V、3.88± 1.40 m V ,Mid较Epi及 Endo的 EADA高 ,差异有显著性 (P<0 .0 1) ;Epi、Mid及 Endo的 EAD耦联间期 (EAD- CI)分别为 131.6 3± 17.43ms,12 5 .2 9± 2 3.6 4m s和 130 .0 5± 19.38ms,Mid较 Epi及 Endo的 EAD- CI小 ,差异有显著性 (P<0 .0 5 ) ,中层心肌的 EAD振幅最高 ,且出现时程最早。12只犬中有 7只出现了恶性室性心律失常 ,均发生于出现 EAD的犬中。再灌注心律失常发生率为 5 8.3%。结论 犬在体心肌再灌注时出现明显 EAD,且 EAD起源于中层心肌细胞 。

粉防己碱对家犬在体心脏单相动作电位的影响

目的:研究粉防己碱(Tet)对家犬在体心室肌单相动作电位(MAP)和有效不应期(ERP)的影响,探讨其抗心律失常的可能机制。方法:家犬14只,随机分为Tet组和维拉帕米(Ver)组,记录右室心内膜MAP及心电图Ⅱ导联,比较不同剂量的Tet和Ver对MAP振幅(MAPA)、复极化达50％和90％一点到MAP上升支的水平距离(MAPD50、MAPD90)、ERP及ERP/MAPD90。结果:Tet引起窦性心率减慢,随剂量增加(3～12 mg/kg)ERP延长、ERP/MAPD90增大,但对MAPA、MAPD50、MAPD90无明显影响;而Ver除延长ERP,增大ERP/MAPD90,还缩短MAPD50、MAPD90。结论:Tet对MAP的影响可能除钙拮抗作用外,还有别的离子基础;延长ERP、增大ERP/MAPD90可能是其抗心律失常的机制。

奎尼丁所致异常U波与早期后除极的相关性研究

静脉注射中毒剂量奎尼丁建立ＱＴＵ间期延长综合征动物模型，应用接触电极导管记录犬左室心内膜单相动作电位（ＭＭ），以研究早期后除极（ＥＡＤ）与Ｕ波的关系。用药后１１条犬体表心电图上均出现异常Ｕ波，同步记录的ＭＡＰ３相上可见高振幅ＥＡＤ，二者振幅高度相关（ｒ＝０．９８），峰值时间基本一致。Ｕ波与ＥＡＤ均具有间歇依赖特性。用药后ＱＴＵ间期由对照的２４０±１９ｍｓ延长至４１５±７４ｍｓ，ＭＡＰ复极至９０％的时间（ＭＡＰＤ＿（９０））由对照的２２３±１８ｍｓ延长至３４８±８２ｍｓ，二者相关良好（ｒ＝０．９８）．用药后，１条犬发生频发成对室性早搏，呈“ＲｏｎＴＵ”现象。ＭＡＰ记录显示提前除极起源于ＥＡＤ峰值近处。无自发性尖端扭转型室性心动过速发生。研究结果表明：ＭＡＰ技术是研究在体心脏抗心律失常药物作用机理的可靠方法；体表心电图上异常Ｕ波可能来源于ＭＡＰ上的ＥＡＤ；ＭＡＰＤ９０是较ＱＴＵ间期更为精确的指标；奎尼丁诱发心律失常机制可能为触发活动。

氯化铯诱发在体心脏触发性心律失常的实验研究

心内膜单相动作电位研究表明,单相动作电位的复极进程能够正确反映心肌细胞动作电位复极时程。狗静脉注射氯化铯后早期后除极电位(EAD)的发生率为100％,单相动作电位90％复极时程明显延长(224.4±50.6ms VS 368.4±34ms),与QT间期延长相一致。氯化铯诱发的室性心律失常发生于EAD顶峰,触发心律联律间期与EAD联律间期密切相关。硫酸镁使EAD和室性心律失常同时消失。提示该心律失常为EAD触发活性所致。