氯沙坦对心房急性电重构的影响

目的　以地尔硫为对照 ,探讨氯沙坦对心房快速起搏诱发急性电重构的干预作用。方法　 2 1只兔随机分为盐水组、地尔硫组和氯沙坦组。 2F电极导管分别置于高位右心房 (HRA)、低位右心房 (LRA)和希氏束区 (HIS) ,以最快 1∶1起搏频率心房起搏 3h。阻断自主神经后 ,观察各组心房快速起搏前后 ,不同部位心房有效不应期 (AERP)、AERP频率适应性、AERP离散度 (AERPd)及右心房内传导时间变化。结果　 (1)心房快速起搏后 ,盐水组AERP2 0 0 和AERP150 立即缩短 ;起搏 1h达最小值(P <0 0 5 ) ,起搏 0 5h内AERP2 0 0 和AERP150 缩短速率最快 [(30 2± 10 5 )ms/h ,(2 4 1± 9 1)ms/h];地尔硫组和氯沙坦组心房快速起搏后AERP无显著缩短。 (2 )心房快速起搏前 ,盐水组HRA处(AERP2 0 0 -AERP150 ) / 5 0ms为 0 17± 0 0 8,起搏 0 5、1、2、3h后分别为 0 0 8± 0 0 6、0 0 9± 0 0 6、0 0 8± 0 0 4、0 0 9± 0 0 5 ,P <0 0 5 ,提示AERP频率适应性降低 ;地尔硫组和氯沙坦组心房快速起搏前后 ,该值差异无显著性。 (3)盐水组心房快速起搏 2、3h ,AERPd明显增大 (P <0 0 5 )。地尔硫组心房快速起搏 3h ,与起搏前比较 ,AERPd显著增大 (P <0 0 5 )。氯沙坦组心房快速起搏后 ,AERPd无显著增加。     

卡托普利对慢性实验犬心房电重构的影响

目的　研究卡托普利对长期快速起搏实验犬心房有效不应期 (AERP)和心房电重构的影响。方法　 2 4只犬随机分为 3组 ,起搏组 :实验犬右颈部皮下植入永久起搏器 ,经颈外静脉途径将起搏电极导线置入右心耳 (起搏频率 4 0 0次 /min)。起搏器植入前及起搏 8周后分别行电生理检查 ,将两条4极电极导管经股静脉途径分别送至右心房高侧壁及右心房前壁 ,作为刺激电极和记录电极 ,以 2个基本周长 (S1=30 0、2 0 0ms)分别标测AERP ;起搏加药物组 :起搏器植入及电生理检查同起搏组 ,起搏器植入前 3d至起搏 8周后 ,每日给予卡托普利 5 0mg 2次 /d口服 ;对照组 :实验犬未植入起搏器 ,仅于相应的时间行电生理检查。结果　起搏组 :起搏 8周后较起搏前 ,AERP明显缩短 [S1=30 0ms,(132 5 0±15 81)msvs(115 0 0± 16 0 3)ms,P <0 0 0 1;S1=2 0 0ms,(12 6 2 5± 10 6 1)msvs(110 0 0± 15 11)ms,P <0 0 0 1];起搏加药物组 :起搏 8周后与起搏前比较 ,AERP无明显变化 [S1=30 0ms,(133 75±15 98)msvs(131 2 5± 13 6 7)ms,P >0 0 5 ;S1=2 0 0ms ,(12 8 75± 12 4 6 )msvs(12 7 5 0± 12 82 )ms ,P>0 0 5 ];对照组 :实验 8周前后所测AERP差异无统计学意义 [S1=30 0ms,(131 2 5± 12 4 6 )msvs(135 0 0± 9 2 6     

依那普利对心房急性电重构影响的临床研究

目的　探讨依那普利对快速心房起搏诱发心房急性电重构的干预作用。方法　 2 7例阵发性室上性心动过速行射频消融术患者随机分为对照组 ( 16例 )和依那普利组 ( 11例 )。阻断自主神经后 ,以最快 1:1心房起搏 [( 349± 37) /min]诱发急性心房颤动 (房颤 ) ,观察各组患者心房快速刺激前后心房有效不应期 (AERP)、AERP频率自适应性、不应期离散度 (AERPd)的变化及房颤诱发情况。结果　①心房快速起搏后 ,对照组AERP明显缩短 ,依那普利组AERP无显著变化。两组患者心房快速起搏前后AERPd差异无显著性 ;②心房快速起搏前后 ,对照组右心耳 (RAA)处AERP与相应程控刺激基础周长拟合直线的斜率分别为 0 0 6 2和 0 0 18;依那普利组分别为 0 0 5 9和 0 0 5 3;③心房快速起搏后 ,对照组房颤诱发例数、次数显著增加 ,平均房颤持续时间明显延长 ;依那普利组心房快速起搏前后房颤诱发情况无显著差异。结论　依那普利能够防止心房快速激动引起的心房急性电重构 ,降低房颤诱发率     

氯沙坦对兔快速心房起搏的电生理作用观察

28只新西兰大耳白兔，随机分为氯沙坦组和对照组各14只。前者灌胃法给予氯沙坦15mg／（kg&#183;d），后者单纯饲料喂养，两组均喂养4周。4周后，颈内静脉切开置入4F电极导管，快速心房起搏1h后，记录起搏前后的心房有效不应期（AERP）；然后猝发S1S1刺激诱发心房颤动（AF），观察AF的诱发率、房颤周长（AFCL）和持续时间。结果①起搏前后AERP缩短值氯沙坦组明显小于对照组[（17．44&#177;5．58）msVS（30．71&#177;8．86）ms，P〈0．01]。②AF的诱发率氯沙坦组少于对照组（28．57％vs85．71％，P〈0．05）。③AF发作的持续时间氯沙坦组短于对照组[（47．5&#177;9．6）sVS（115．0&#177;8．0）s，P〈0．01]。④AFCL氯沙坦组长于对照组[（85．0&#177;10．0）msvs（45．0&#177;8．0）ms，P〈0．01]。认为氯沙坦能阻止兔快速心房起搏引起的AERP缩短和诱发AF等心房电重构现象。     

建立犬心房颤动模型的研究

用自制健索钩刀破坏25条犬部分二尖瓣腱索，造成中等程度二尖瓣关闭不全，建立心房颤动（AF）动物模型。术后12周内每2周1次行超声心动图及电生理检查，每次检查后用Burst刺激法诱发AF。术后2周左房前后径增加（22．70±2．31mmvs20．39±3．08mm，P＜0．05），术后4周左房面积增加（7．01±1．91cm2vs5．63±2．05cm2，P＜0．05）。术后4周P波时限延长（61．00±5．07msvs48．75±8．82ms）、高位右房有效不应期缩短（102．67±11．00msvs133．33±14．97ms），P均＜0．01。术后12周80％（8／10）的犬可诱发出持续时间＞5min的AF。左、有房AF波周期无显著差异（102．50±17．89msvs116．60±18．24ms，P＞0．05）。通过破坏二尖瓣腱索造成犬急性二尖瓣关闭不全，手术后随时间延长，动物表现在房扩张及右房有效不应期缩短和心房内传导时间延长，此与临床上瓣膜病引起的AF有一定的对应性，因而是研究AF电生理的良好模型。     

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。     

房间隔起搏对阵发性心房颤动患者最大P波时限和P波离散度的影响

观察房间隔起搏对阵发性心房颤动 (AF)患者最大P波时限 (Pmax)及P波离散度 (Pd)的影响 ,探悉房间隔起搏防治AF发作的电生理机制。对 2 1例阵发性AF患者和 2 6例室上性心动过速行射频消融术无阵发性AF患者 ,分别进行右心耳和房间隔起搏 ,比较不同部位起搏对阵发性AF和无阵发性AF患者的Pmax和Pd影响。结果 :阵发性AF患者较无阵发性AF患者Pmax和Pd值明显大 (分别为 1 35± 1 5vs 1 1 9± 1 4ms ,P <0 .0 5 ;36 .5± 9.2vs 1 9.7± 7.1ms ,P <0 .0 1 ) ;房间隔起搏使阵发性AF患者Pd、Pmax显著下降 (分别为 2 3 .4± 8vs 36 .5± 9.2ms ,1 2 0± 1 1vs1 35± 1 5ms,P均 <0 .0 5) ;右心耳起搏使无阵发性AF患者Pmax和Pd明显增加 (分别为 1 32± 1 2vs 1 1 9± 1 4ms,2 5 .5± 8.5vs 1 9.7± 7.1ms ,P均 <0 .0 5)。结论 :右心耳起搏能够使无阵发性AF患者Pmax和Pd值增加。房间隔起搏能够明显降低阵发性AF患者Pmax、Pd ,纠正房内或房间传导延缓 ,改善心房内电活动的各向异性 ,防治AF发作     

腹主动脉结扎大鼠房性快速心律失常诱发率升高

研究腹主动脉结扎大鼠心房颤动 (AF)和房性心动过速 (AT)诱发率的改变。雄性SD大鼠随机分为非手术对照组 (C组 ,n =1 2 ) ,腹主动脉结扎组 (AB组 ,n =1 2 )和腹主动脉结扎 +依那普利组 (AB E组 ,n =1 2 ) ,C组和AB组按常规方法喂养 ,AB E组于术后第 2天加喂依那普利 (2 0mg/Kg ,放于饮水中 ) ,三组喂养时间均为 4周。 4周后动物麻醉 ,描记I导体表心电图 ,经左侧颈总动脉插管测量收缩压和舒张压。在心脏体外灌流条件下 ,采用心房短阵刺激评价房间传导时间 (IACT)和心房对刺激的反应。取心房组织制作切片 ,Masson染色 ,测量纤维组织占总区域的百分比。结果 :AB组AngⅡ水平较C组明显升高 (1 .76± 0 .5ng/mlvs 0 .97± 0 .4ng/ml,P <0 .0 1 ) ,P波持续时间和IACT也较C组延长 (分别为 2 7.8±5 .1msvs2 3± 4 .5ms,P <0 .0 5和 37.3±5msvs 2 3.1± 3.3ms,P <0 .0 1 ) ,在AB组诱发出 4例AF和 3例AT ;AB E组AngⅡ水平较AB组明显降低 (1 .1 2± 0 .3ng/mlvs 1 .76± 0 .5ng/ml,P <0 .0 5 ) ,P波持续时间和IACT也较AB组缩短 (分别为 2 2± 4 .1msvs 2 7.8± 5 .1ms ,P <0 .0 5和 2 2 .6± 3msvs 37.3± 5ms,P <0 .0 1 ) ,仅诱发出 2例AT ;C组没能诱发出AF和AT。组织学发现AB组较C组有明显的纤维化 ,AB E组纤维?     

心房颤动电重构的实验研究

目的 :研究犬心房颤动 (Af)模型心房有效不应期 (ERP)的变化 ,验证Af电重构这一假说的正确性。方法 :采用快速心房起搏的方法建立犬的Af模型 (起搏组 ,n =13) ,用程序刺激测量心房的ERP ;观察P波时限和PA间期的变化 ,并与假手术组 (对照组 ,n =7)作比较。结果 :持续快速起搏 9～ 10周后 ,心房ERP明显缩短 ,当S1S1为 30 0ms时 ,对照组与起搏组分别为 (15 0± 2 1)ms与 (115± 2 3)ms(P<0 .0 1) ;S1S1为 4 0 0ms时分别为(15 4± 2 4 )ms与 (10 5± 2 7)ms(P <0 .0 1)。起搏组P波时限和PA间期明显长于对照组。结论 :持续心房快速刺激可使ERP明显缩短 ,使心房发生电重构。心房电重构可促进Af的发生和发展     

去迷走神经效应对心房颤动作用的实验研究

目的探讨去迷走神经效应在心房颤动中的作用。方法将16只成年健康犬随机分成切除脂肪垫组和保留脂肪垫组,心外膜缝植动物起搏器后快速起搏犬心房,观察两组心房有效不应期（AERP）及其离散度（AERPd）、心房颤动诱发率、持续时间等。结果两组持续心房起搏6周后,起搏器停止工作0、3、7h,保留脂肪垫组AERP和AERPd分别为（115±19）ms、（126±24）ms、（132±19）ms和（440±55）ms、（480±47）ms、（40±69）ms,与起搏前比较差异均有统计学意义（P〈0．05）,与保留脂肪垫组比较差异均无统计学意义（P〉005）。保留脂肪垫组持续性心房颤动诱发率714％,持续时间（52±62）min,阵发性心房颤动持续时间明显延长,切除脂肪垫组未诱发出持续性心房颤动。结论去迷走神经可减少实验犬心房颤动诱发率及控制持续时间。     

用实验性心力衰竭制作持续性心房颤动模型

为探讨实验性心力衰竭（简称心衰）形成持续性心房颤动（简称房颤）的可行性，用２００～２５０ｐｐｍ的频率以ＶＯＯ方式起搏犬心室３～７周形成实验性心衰，在犬清醒状态下观察心衰前、后刺激诱发的房性快速心律失常。快速起搏右室３～７周，８条犬均发生充血性心衰，３周时体重由心衰前的２８±６ｋｇ降至２４±４ｋｇ（Ｐ＜０．０５）；左室射血分数由０．６４±０．０６降至０．２３±０．０９（Ｐ＜０．０１），右房直径由２５±３ｍｍ增至３６±６ｍｍ（Ｐ＜０．０１），心房不应期由１１６±５ｍｓ增至１３７±１２ｍｓ（Ｐ＝０．０１），不应期离散度无显著性改变（１６±１２ｍｓｖｓ２０±９ｍｓ，Ｐ＝０．２０），心房平均传导时间亦无显著性变化（６１±１９ｍｓｖｓ６６±２４ｍｓ，Ｐ＝０．２０）。１条犬于起搏后第６周夜间突然死亡。心衰前，８条犬均未诱发心房扑动，４条犬诱发短暂房颤；心衰后，８条犬均可反复诱发心房扑动和持续性房颤（持续时间超过１５ｍｉｎ，平均周长９５±５ｍｓ），最长者持续２４ｈ以上。结果表明起搏心室导致犬心衰可形成非瓣膜病性慢性房颤的实验模型。     

Effect of pilsicainide on atrial electrophysiologic properties in the canine rapid atrial stimulation model.

The heterogeneous process of atrial electrical remodeling (AER) in the canine rapid atrial stimulation model has been previously reported although it has been reported that a sodium channel blocker might suppress the shortening of the atrial effective refractory period (AERP), its effect on long-term electrical remodeling is unknown. In the present study, the effect of pilsicainide on AER was evaluated. The right atrial appendage (RAA) was paced at 400 beats/min for 2 weeks. In the RAA, Bachmann's bundle (BB), the right atrium near the inferior vena cava (IVC) and in the left atrium (LA), AERP, AERP dispersion (AERPd) and the inducibility of atrial fibrillation (AF) were evaluated at several time points of the pacing phase and the recovery phase (1 week). The same protocol was performed during the administration of pilsicainide (4.5 mg/kg per day) and the parameters were compared with the controls. In the control dogs, the AERP was significantly shortened by rapid pacing at all atrial sites studied and the AERP shortening (DeltaAERP) was larger at the RAA and LA sites (p<0.03). However, pilsicainide decreased these DeltaAERPs at all 4 atrial sites. AERPd was increased during the pacing phase whereas it was decreased during the recovery phase in the control dogs. In contrast, this pacing-induced AERPd was attenuated by the administration of pilsicainide. The AF inducibility was highest at the LA site in both groups, and the inducibility was lower in the pilsicainide group than the control group at all atrial sites. During the rapid pacing phase, the ventricular heart rate was significantly lower in the pilsicainide group than the control because of intra-atrial conduction block. In a canine rapid right atrial stimulation model, pilsicainide suppressed the shortening of the AERP at all atrial sites, possibly through the improvement of the hemodynamics as well as the action of the Na - Ca exchanger.     

肾去交感神经对犬心房颤动易患性和心房重构的影响

目的 探讨肾去交感神经对犬长期快速右心房起搏后心房颤动（房颤）易患性和心房重构的影响.方法 20只杂种犬分为假手术组、右心房起搏（RAP）组、肾去交感神经（RSD）组3组.假手术组（n=6）植入起搏器后程控关闭起搏器;RSD组（n=7）先行双侧肾交感神经消融,经6周恢复后植入起搏器;RAP组（n=7）和RSD组快速起搏（400～ 450次/min）右心房5周.所有犬在实验基线期和终点进行超声心动图及电生理检查,取静脉血检测血管紧张素Ⅱ（AngⅡ）水平;处死动物后迅速取心房组织行形态学评估.结果 与假手术组和RSD组相比,RAP组犬起搏5周后房颤诱发率明显升高（P＜0.05）.RAP组心房有效不应期（AERP）明显缩短[（142±8）ms对（115±9）ms,P＜0.05],而RSD组AERP缩短无统计学意义（P＞0.05）.超声心动图结果发现,RAP组和RSD组的左心房内径（LAD）、左心室舒张末期内径（LVEDD）、左心房容积最大值和最小值（LAVmax和LAVmin）起搏5周后均较起搏前明显增加,但RSD组的LAVmax和LAVmin较RAP组明显减少（P＜0.05）.右心房快速起搏5周后,与假手术组相比,RAP组和RSD组犬血清AngⅡ水平明显增加[RAP组：（217.5±53.5） ng/L对（95.0±25.2） ng/L,P＜0.05;RSD组：（149.6±26.3）ng/L对（95.0±25.2） ng/L,P＜0.05];与RAP组相比,RSD组犬血清AngⅡ显著降低（[（149.6±26.3）ng/L对（217.5±53.5） ng/L,P＜0.05）.电镜结果显示肾去交感神经能显著减缓快速右心房起搏5周后导致的肌丝分解、肌纤维带型和收缩完整结构的丧失和线粒体肿胀等超微结果变化.Masson三色法染色结果表明与RAP组相比,RSD组犬左、右心房肌的胶原容积分数（CVF）均明显减低（P＜0.05）.结论 肾去交感神经可抑制长期快速右心房起搏后房颤的诱发和心房重构.     

Inhomogeneity in the appearance of electrical remodeling during chronic rapid atrial pacing: evaluation of the dispersion of atrial effective refractoriness

In the present study, the long-term process of progression of electrical remodeling at various atrial sites, which is not well understood, was compared while monitoring continuously the electrophysiologic parameters at multirecording sites in canine atria during continuous atrial burst pacing. A rapid pacing device was implanted in 5 dogs, and continuous atrial burst pacing (400 beats/min) was delivered at the right atrial appendage (RAA). Four pairs of epicardial wire electrodes were sutured on (1) the RAA, (2) Bachmann's bundle (BB), (3) the right atrium close to the inferior vena cava (IVC), and (4) the left atrium (LA). The distal ends of those wires were exteriorized posteriorly and used for pacing and recording. The atrial effective refractory period (AERP), AERP dispersion (AERPd), atrial conduction time (CT) and inducibility of atrial fibrillation (AF) were evaluated during burst pacing for 14 days and during the subsequent 7 days' recovery. The AERP at the LA pacing site was shorter than that at the other sites on day 0. The AERP shortening was greater in the RAA and LA sites than in the BB and IVC sites. The AERPd increased during pacing and reached the maximum level on day 3, and then decreased during the recovery phase. Prolongation of CT tended to be longer between the RAAand IVC sites than that between the other sites. The incidence of AF induction became higher in accordance with the time course of the rapid pacing phase. There was another peak of AF induction on days 7-10. In a canine chronic rapid atrial stimulation model, the progression of electrical remodeling (ie, the shortening of the AERP and the prolongation of the CT) was not homogeneous in both atria, the AERPd showed a temporal increase between days 3 and 7 and matched the increase in AF inducibility at the LA pacing site, the increase in the AERPd was mainly caused by more rapid AERP shortening at the RAA or LA sites, and the LA site always showed a shorter AERP than the other atrial sites in the control state and during the rapid pacing phase, whereas AF inducibility was higher at the LA site than the other sites.     

风心病慢性房颤心外膜标测心房有效不应期的对比研究

目的:研究风心病慢性房颤的电生理特征。方法:对29例风心病伴或不伴慢性房颤的病人在行二尖瓣置换术时,采用心外膜标测技术测定左、右心房各部位的有效不应期(AERP)及右房内和房间的传导时间。结果:风心病慢性房颤组左、右心房AERP比窦性心律明显缩短(P<0.05),左、右心房各部分的AERF,之间有明显差异(P< 0.01),即存在明显离散性;慢性房颤组的右房和房间传导时间在转复为窦性心律和缩短刺激右房高位问期时均显著长于正常对照组(P<0.05)。结论:风心病慢性房颤心房各部位AERP的差异反映了其AERP的离散性,而AERP 的离散性在房颤的诱发和维持过程中起着重要作用。     

Consequences of atrial electrical remodeling for the anti-arrhythmic action of class IC and class III drugs

OBJECTIVE: Atrial fibrillation (AF) induces electrical and ionic remodeling of the atria. We investigated whether AF-induced remodeling alters the electrophysiological and anti-fibrillatory effects of class I (flecainide) and class III (d-sotalol, ibutilide) anti-arrhythmic drugs. METHODS: In 9 goats, the effects of flecainide (6 mg/kg) and d-sotalol (6 mg/kg) on atrial electrophysiology were measured both before and after 48 h of electrically induced AF. During a 1-h infusion period the atrial effective refractory period (AERP) and conduction velocity (CV) were measured both during slow and rapid pacing (interval 400 and 200 ms). In 8 other goats, the rate-dependent effects of ibutilide (0.12 mg/kg) on AERP were determined. RESULTS: The effects of flecainide on atrial conduction and refractoriness were not altered after 48 h of AF. At a dose of 6 mg/kg flecainide reduced the CV200 by 19+/-5% in normal atria and by 21+/-9% after 48 h of AF (p=0.20). The AERP200 was prolonged by 10+/-6% and 8+/-7%, respectively (p=0.40). In contrast, the effect of d-sotalol on atrial refractoriness was markedly diminished. During control d-sotalol prolonged the AERP400 by 17+/-6% compared to only 6+/-5% after 2 days of AF (p<0.01). Also ibutilide lost much of its class III effect on the AERP by electrical remodeling (from 15 to 5%; p<0.05). The loss of class III action was less pronounced at rapid heart rates. CONCLUSIONS: AF-induced atrial electrical remodeling in the goat did not modulate the action of flecainide on atrial conduction and refractoriness. In contrast, the class III effects of d-sotalol and ibutilide on the atria were strongly reduced after 2 days of AF. The prolongation of QT-duration was not affected.     

环孢素A对心房颤动犬心房L型钙离子通道蛋白αlc亚单位的影响

目的 研究环孢素A(CsA)作用下心房颤动(房颤)犬心房电生理特性及心房L型钙离子通道蛋白αlc亚单位(Lαle)表达变化.方法 实验犬分为CsA组、房颤组及假手术组(Sham组),快速起搏心房建立犬房颤模型,记录标测并对比各组起搏前后P波时程、心房有效不应期(AERP)的差异,应用Western blot免疫印迹技术比较各组问Lαlc表达的差异.结果 房颤组、CsA组较Sham组P波时程延长(P<0.05),AERP缩短P<0.05).CsA组较房颤组AERP延长(P<0.05).房颤组较Sham组Lαlc表达明显降低(P<0.01).CsA组较房颤组Lede升高(P<0.01),CsA组与Sham组之间差异无统计学意义.结论 CsA 应用逆转了房颤犬心房Lαlc表达变化并改善了心房电生理重构,可能会在房颤的治疗中发挥积极的意义.     

热休克蛋白70 mRNA表达上调对兔心房快速起搏电重构的影响

目的：探讨热应激诱导心肌热休克蛋白70（HSP70）mRNA表达上调后,对兔快速心房起搏电重构的影响。方法：将24只新西兰大白兔随机分成热应激＋起搏组（n=8）、起搏组（n=8）和假手术组（n=8）。热应激造模：将新西兰大白兔麻醉后,放入恒温箱中加热,肛温达41℃后持续15 min,再放入室温恢复24 h。起搏：以600次/min行右心房起搏,测量0 h、2 h、4 h、6 h的右房有效不应期（AERP200、AERP150）,AERP频率适应性,心房颤动（AF）诱发率。起搏组对未造模的兔起搏。假手术组只测量不起搏。用逆转录聚合酶链式反应（RT-PCR）检测各组心肌HSP70 mRNA含量。结果：（1）快速心房起搏后,起搏组AERP200和AERP150立即缩短,起搏2h接近最小值[AERP200（79.38±6.23）ms,AERP150（71.25±6.94）ms],较起搏前[AERP200（100.00±6.55）ms,AERP150（89.38±6.78）ms]显著缩短（P〈0.01）;热应激＋起搏组起搏前后AERP无显著变化;（2）0 h时,起搏组右心房处（AERP200-AERP150）/50 ms为（0.21±0.10）ms,起搏2 h、4 h、6 h后分别为（0.16±0.07）、（0.14±0.05）、（0.13±0.05）ms,较起搏前非常显著缩短（P〈0.001）;（3）快速心房起搏前,予以程序性刺激和猝发刺激,各组AF诱发率均为0,起搏后2 h、4 h、6 h AF诱发率：起搏组分别为50.0%、75.0%、87.5%;热应激＋起搏组分别为25.0%、25.0%、37.5%;较起搏组显著减少（P〈0.05）;（4）热应激＋起搏组心脏各部位HSP70 mRNA表达较起搏组和假手术组明显增高（P〈0.05）,起搏组和假手术组间无显著差异。结论：心脏热休克蛋白70 mRNA表达上调后可抑制右心房快速起搏引起的心房电重构。     

Regional differences in the recovery course of tachycardia-induced changes of atrial electrophysiological properties

BACKGROUND: Regional differences in recovery of tachycardia-induced changes of atrial electrophysiological properties have not been well studied. METHODS AND RESULTS: In the control group (5 dogs), atrial effective refractory period (AERP) and inducibility of atrial fibrillation (AF) were assessed before and every 4 hours for 48 hours after complete atrioventricular junction (AVJ) ablation with 8-week VVI pacing. In experimental group 1 (15 dogs), AERP and inducibility of AF were assessed before and after complete AVJ ablation with 8-week rapid right atrial (RA) pacing (780 bpm) and VVI pacing. In experimental group 2 (7 dogs), AERP and inducibility of AF were assessed before and after 8-week rapid left atrial (LA) pacing and VVI pacing. AERP and inducibility and duration of AF were obtained from 7 epicardial sites. In the control group, atrial electrophysiological properties obtained immediately and during 48-hour measurements after pacing did not show any change. In the 2 experimental groups, recovery of atrial electrophysiological properties included a progressive recovery of AERP shortening, recovery of AERP maladaptation, and decrease of duration and episodes of reinduced AF. However, recovery of shortening and maladaptation of AERP and inducibility of AF was slower at the LA than at the RA and Bachmann's bundle. CONCLUSIONS: The LA had a slower recovery of tachycardia-induced changes of atrial electrophysiological properties, and this might play a critical role in initiation of AF.