血管紧张素-（1-7）对快速心房起搏犬心房重构及p38MAPK蛋白表达的影响

目的:观察快速心房起搏后犬心房重构与p38MAPK蛋白激活的关系,以及血管紧张素（Ang）-(1-7)的干预作用。方法:普通杂种犬15只随机分为3组,假手术组（Sham,S组）、心房起搏组（Pacing,P组）和心房起搏+Ang-(1-7)组（A组）,每组5只,所有犬均安置心房起搏器,除假手术组外,其余两组均给予500次/min持续右心房起搏,A组以6 μg/（kg·h）连续给予Ang-（1-7）,起搏2周后分别测定各组犬的心脏结构变化、心房有效不应期、房颤诱发率及持续时间,HE染色及Masson染色观察心房肌细胞结构变化,Western blot技术测定左心房组织p38MAPK、磷酸化p38MAPK的蛋白表达情况。结果:与假手术组比较,心房起搏组左室射血分数降低,心房有效不应期缩短,房颤诱发率及持续时间升高,心肌细胞排列紊乱,细胞间纤维组织增多,磷酸化p38MAPK水平明显升高（P＜0.05),Ang-(1-7)组较心房起搏组左室射血分数、心房有效不应期、房颤诱发率及持续时间均明显改善,磷酸化p38MAPK蛋白降低（P＜0.05）,但p38MAPK在3组间的差异未达到统计学意义。结论:快速心房起搏导致的心房重构与p38MAPK磷酸化激活有关,Ang-（1-7）可通过降低p38MAPK激活而保护心房重构。     

Effects of Losartan on acute atrial electrical remodeling

Background Atrial electrical remodeling (AER) contributes to the maintainance of atrial fibrillation (AF). This study was to compare the effects of Losartan with those of Diltiazem on tachycardia-induced acute AER in rabbits.Methods Twenty-one rabbits paced with maximal atrial capture rate for 3 hours in the right atrium (RA) were randomly divided into saline group, Diltiazem group and Losartan group. After autonomic blockage, we measured atrial effective refractory period (AERP), AERP rate adapting feature, AERP dispersion and RA conduction time at basic cycle lengths (BCLs) of 200 ms and 150 ms at baseline, 0.5 hour, 1 hour, 2 and 3 hours after rapid atrial pacing. Results In the saline group, there was a prompt decrease in AERP as a result of rapid atrial pacing, and AERP200 and AERP150 were shortened sharply within 0.5 hour of pacing （30.2±10.5 ms and 24.1±9.1 ms, respectively）. The AERP did not change dramatically in the Diltiazem and Losartan groups. In the saline group, the value of （AERP200-AERP150）/50 ms in high RA was 0.17±0.08 at baseline and became significantly smaller at 0.5 hour (0.08±0.06), 1 hour (0.09±0.06), 2 hours (0.08±0.04) and 3 hours (0.09±0.05) (all P<0.05), suggesting a reduction of rate adaptation of AERP. The value of （AERP200-AERP150）/50 ms in high RA did not change during the 3 hours of pacing in both Diltiazem and Losartan groups. In the saline group, AERP dispersion increased significantly at 2 and 3 hours (P<0.05). However, Diltiazem could not prevent the increase of AERP dispersion at 3 hours (P<0.05). During Losartan infusion, the AERP dispersion was no longer increased after rapid atrial pacing. There was no significant difference in RA conduction time among the three groups.Conclusion Like calcium antagonist Diltiazem, Losartan could prevent AERP shortening and preserve rate adaptation of AERP after rapid atrial pacing. Losartan is more effective than Diltiazem in inhibiting the increase of AERP dispersion.     

导管消融去肾交感神经抑制星状神经节刺激诱发的心房颤动

【目的】探讨经导管射频消融去肾交感神经对交感神经过度激活介导的心房颤动的影响和心房电重构机制?【方法】 16只家犬随机分为对照组(n = 8)和去肾交感神经(RSD)组(n = 8),RSD组进行经导管射频消融去肾交感神经术,对照组行不消融肾交感神经的假手术,通过左侧星状神经节电刺激(LSG) +快速心房起搏(RAP)3 h建立交感神经介导的房颤犬模型?【结果】 LSG刺激联合RAP使左心耳?右心房?左上肺静脉?左下肺静脉部位的房颤诱发率升高,有效不应期缩短(ERP),有效不应期离散度增大,均较基础值有统计学差异(P < 0.05),RSD组消融后各部位房颤诱发率降低?ERP显著延长?ERP离散度显著缩小,与对照组相比有统计学差异(P < 0.05)?LSG刺激联合RAP引起各检测部位的R-R间期?SDNN缩短,LF?HF和LF/HF降低,均较基础值有统计学差异(P < 0.05);RSD可逆转LSG刺激联合RAP引起的这些心率变异性改变,与对照组相比具有统计学差异(P < 0.05)?【结论】 交感神经过度激活使房颤易于诱发?恶化急性心房电重构,RSD可有效降低房颤的诱发率,抑制心房电重构?改善心脏自主神经功能,提示RSD对交感神经过度激活介导的房颤的发生具有潜在抑制作用?     

螺内酯对快速起搏家兔心房电重构的影响

目的观察醛固酮受体拮抗剂——螺内酯对快速心房起搏家兔心房电重构的影响。方法将30只家兔随机分为3组,对照组、快速起搏组及螺内酯组各10只。经颈内静脉将心房电极置入右心房。分别测量起搏开始前、起搏开始后1h、2h、4h、6h、8h分别记为（P0、P0、P2、P4、P6、P8）时的心房有效不应期（AERP200和AERP150）。结果快速起搏组在不同基础刺激作用下AERP缩短,AERP200-AERP150频率适应性不良,P。与起搏前P。比较差异有统计学意义（P〈0．05）,螺内酯组AERP缩短较快速起搏组减轻,频率适应性得以维持（P〉0．05）。结论螺内酯可以抑制快速心房起搏所致电重构。     

川芎嗪对心室快速起搏心力衰竭实验犬心房颤动及心房纤维化的影响

目的:观察川芎嗪(tetra methyl pyrazine,TMP)对心室快速起搏致充血性心力衰竭(congestive heart failure,CHF)实验犬心房颤动及心房纤维化的影响。方法:选择健康成年杂种犬21只,随机分为正常对照组、CHF模型组和TMP治疗组。采用右心室快速起搏建立实验犬CHF模型。Burst刺激诱发心房颤动(atrial fibrillation,AF)。超声心动图仪检测实验犬左心室射血分数(left ventricular ejection fraction,LVEF)。Mallory’s三色法染色检测心房组织纤维化程度。采用放射免疫法测定血浆血管紧张素Ⅱ和醛固酮的浓度,测定血清Ⅲ型前胶原氨基末端肽(amino-terminal peptide of typeⅢ procollagen,PⅢNP)、层粘连蛋白(laminin,LN)和透明质酸(hyaluronic acid,HA)的水平。结果:CHF模型组LVEF较正常对照组明显下降(P<0.01);AF发生率、持续性AF发生率及AF持续时间较正常对照组均明显增加(P<0.01);左右心房纤维化程度较正常对照组亦有明显增加(P<0.01);AF持续时间与左心房纤维化程度呈密切正相关(r=0.84,P=0.018);血浆血管紧张素Ⅱ、醛固酮以及血清PⅢNP、HA水平较正常对照组均有明显升高(P<0.05,P<0.01);LN比较则无统计学差异;血浆血管紧张素Ⅱ水平与醛固酮水平呈密切正相关(r=0.759,P=0.048)。TMP治疗组LVEF较CHF模型组有明显改善(P<0.05);持续性AF发生率较CHF模型组有明显降低(P<0.05);左右心房纤维化程度较CHF模型组有明显减轻(P<0.01)。结论:TMP可减轻CHF时心房纤维化的程度,这可能是其减少CHF时AF发生率及持续时间的机制之一。     

家兔急性房颤模型的建立

目的探讨经快速肺静脉起搏方法制作家兔急性心房颤动（房颤）动物模型的可行性。方法64只家兔随机分为实验组（n=32）及对照组（n=32）,对照组为假手术组通过开胸植入食道调搏电极但不起搏,实验组通过开胸植入食道调搏电极（程序刺激与Burst刺激相结合）刺激肺静脉建立家兔急性房颤模型,监测房颤的发生情况、持续时间及房颤时心室率变化情况,同时测定起搏前及房颤发生后心房有效不应期（AERP）的变化,并对心房组织超微结构进行观察。结果实验组经程序刺激诱发出房颤15只,爆发刺激诱发出房颤8只,房颤总诱发率为71．88％;对照组2只发生房颤,房颤发生率为6．25％。实验组房颤持续时间（40．53±3．70）min,对照组（17．05±1．55）min,两者比较有显著性差异（P〈0．01）。房颤时心室率[（307．64±2．74）次／min]明显快于基础心率[（227．70±1．02）次／min],有显著性差异（P〈0．01）;AERP缩短,AERP频率适应不良,与基础状态相比有统计学意义（P〈0．05）。实验组光镜下左心房组织切片HE染色观察到早期炎症表现。结论经快速肺静脉起搏方法制作房颤动物模型成功率高、重复性好,是建立急性房颤模型的有效方法。     

比格犬与杂种犬右心室快速起搏至房颤模型比较

目的 比较比格犬和杂种犬制作的右心室快速起搏至房颤模型,选择出表达更加稳定的房颤动物模型.方法 雌性杂种犬与比格犬各8只采用完全随机设计,将8只杂种犬分为2组,每组4只,记为杂种犬对照组与杂种犬实验组;将8只比格犬分为2组,每组4只,记为比格犬对照组与比格犬实验组.各实验组在X线透视下,经颈外静脉将1条心室起搏电极植入右心室心尖.连接心室起搏电极与起搏器,起搏器埋于右侧颈部皮下.以240次/min快速起搏心室,送回动物房饲养.2周后测定血流动力学指标和电生理指标,处死,快速取出心脏,测定心脏重量等相关指标.结果 比格犬在心率,心脏系数,左心室内压这几个指标中与杂种犬比较差异均无统计学意义;比格犬对照组与杂种犬对照组心房不应期无明显差别;杂种犬实验组右心室快速起搏后心房不应期有下降趋势,但差异无统计学意义;比格犬实验组右心室快速起搏后心房不应期下降,差异有统计学意义（P＜0.01）;比格犬对照组与杂种犬对照组比较,房颤诱发率差异有统计学意义（P＜0.05）.结论 比格犬较杂种犬在右心室快速起搏至房颤模型中表达稳定,效果明显,有一定优势.     

Probucol attenuates atrial autonomic remodeling in a canine model of atrial fibrillation produced by prolonged atrial pacing

Background We hypothesize that increased atrial oxidative stress and inflammation may play an important role in atrial nerve sprouting and heterogeneous sympathetic hyperinnervation during atrial fibrillation （AF）. To test the hypothesis, we examined whether the antioxidant and anti-inflammatory treatment with probucol attenuates atrial autonomic remodeling in a canine model of AF produced by prolonged rapid right atrial pacing.
Methods Twenty-one dogs were divided into a sham-operated group, a control group and a probucol group. Dogs in the control group and probucol group underwent right atrial pacing at 400 beats per minute for 6 weeks, and those in the probucol group received probucol 1 week before rapid atrial pacing until pacing stopped. After 6-week rapid atrial pacing, general properties including left atrial structure and function, atrial hemodynamics and the inducibility and duration of AF were measured in all the groups. Atrial oxidative stress markers and serum C-reactive protein （CRP） concentration were estimated. The degree of nerve sprouting and sympathetic innervation at the right atrial anterior wall （RAAW） and the left atrial anterior wall （LAAW） were quantified by immunohistochemistry, atrial norepinephrine contents were also detected. Atrial beta-nerve growth factor （beta-NGF） mRNA and protein expression at the RAAW and LAAW were assessed by real-time quantitative RT-PCR and Western blotting respectively.
Results Atrial tachypacing induced significant nerve sprouting and heterogeneous sympathetic hyperinnervation, and the magnitude of nerve sprouting and hyperinnervation was higher in the RAAW than in the LAAW. Atrial beta-NGF mRNA and protein levels were significantly increased at the RAAW and LAAW, and the upregulation of beta-NGF expression was greater at the RAAW than at the LAAW in the control group. The beta-NGF protein level was positively correlated with the density of sympathetic nerves in all groups. Probucol decreased the increase of CRP concentration and attenuated atrial oxidative stress caused by atrial tachypacing. In addition, probucol could effectively inhibit atrial beta-NGF upregulation, significantly attenuate atrial nerve sprouting and heterogeneous sympathetic hyperinnervation, and dramatically reduce the inducibility and duration of AF.
Conclusions The atrial over-expression of beta-NGF possibly caused by increased oxidative stress and inflammation may be the main mechanism underlying atrial autonomic remodeling during AF. Probucol attenuates atrial autonomic remodeling possibly by its antioxidant and anti-inflammatory actions.     

Effect of nifekalant on acute electrical remodelling in rapid atrial pacing canine model

Atpresent, treatment of atrial fibrillation (AF) with antiarrhythmic drugs is problematic, a better understanding of the mechanisms determining antiarrhythmic drug efficacy would help in improving therapy.1 Recent evidence indicates that disease or arrhythmic induced alterations in cardiac electrophysiology (electrical remodelling) are central in arrhythmic genesis, Aparticularly for AF, which alters cardiac electrophysiology to promote its own maintenance.2,3 Pharmacological therapy to prev…     

两种不同起搏模型心房颤动发生机制的比较

目的对比心房快速起搏（ATP）与心室快速起搏（VTP）诱发心房颤动（AF）起搏模型的电重构和结构重构,探讨其（特别是VTP模型）导致的充血性心力衰竭（CHF）与AF发生维持的关系.方法选择健康成年杂种犬21只,随机分为对照组、ATP组和VTP组.采用Burst刺激诱发AF,心房有效不应期（ERP）采用S1S2法,超声心动图测定左右心房收缩末期面积,Mallory三色法染色并测定纤维化百分比.结果VTP组的左室射血分数显著降低;ATP组与VTP组AF诱发率、持续性AF诱发率均明显增加,AF持续时间明显延长,ATP组ERP显著缩短且频率自适应性几乎消失,AF持续时间与ERP呈密切负相关.VTP组与对照组ERP及其频率自适应性无明显变化,但VTP组左右心房明显扩大,纤维化程度显著增高,AF持续时间和左心房收缩面积及左心房纤维化程度呈密切正相关.结论ATP模型的AF发生、维持主要与电重构有关,VTP模型导致CHF时AF发生、维持的重要因素可能是心房扩大及心房纤维化等结构性重构.     

Cariporide和维拉帕米防止家兔快速心房起搏所致电重构

目的 探讨家兔快速心房起搏所致的心房肌电重构的机制及钠氢离子交换体抑制剂Cariporide和L型钙通道阻断剂维拉帕米的防治效果。方法 36只家兔随机分为3组:快速心房起搏对照组(对照组)、快速心房起搏 Ca-riporide组(Cariporide组)、快速心房起搏 维拉帕米组(维拉帕米组),每组12只。经颈内静脉将电极置入右心房,以600次/min行快速心房起搏,测定基础状态、给药后0.5 h和起搏后0.5、1、2、4、6、8 h的心房有效不应期(AERP200、AERP150和AERP130),取起搏8 h的兔右心耳组织,观察超微结构。结果 快速心房起搏后对照组的AERP缩短,AERP的频率适应不良,同基础状态比较差异有显著性意义(P<0.01),心房肌细胞损伤的超微结构变化明显。Cariporide组和维拉帕米组上述改变得以逆转和减轻。结论 心房肌细胞内钙水平的增高在快速起搏导致的心房肌电重构中起作用,钠氢离子交换体活化是引起钙超载的原因之一。     

快速左心耳起搏对犬心房构型、心功能及病理组织学特点改变的时间进程研究

目的 探讨慢性心房颤动(Atrial Fibrillation,AF)犬随时间进程心房构型、心功能、病理组织学及超微结构的变化特点.方法 14只比格犬随机分为起搏组(n=7)和对照组(n=7),于左心耳缝植起搏电极,连接实验用VOO型起搏器(频率为400次/min),快速持续起搏8周,建立犬慢性AF模型.分别于0、1、2、4、6、8周时应用超声心动图测量左房横径及心室射血分数,实验结束后取心房肌组织用光镜和电镜观察心房肌的超微结构.结果 (1)心脏超声结果显示8周的左房内径与起搏前比较明显增加,差异有统计学意义(P<0.01),在起搏1周时左房内径已经明显增加,随后2、4、6、8周的左房内径出现逐渐增加趋势.同时,起搏8周心室射血分数与起搏前相比显著降低,差异有统计学意义(P<0.01),心室射血分数1周时已经明显降低,与起搏前比较,差异有统计学意义(P<0.01),随后2、4、6、8周心室射血分数出现逐渐降低趋势.而对照组起搏电极植入前后均未发生明显变化.(2)起搏犬心房肌细胞明显肥大,变性,心肌纤维排列紊乱,线粒体增多、体积变大,细胞间存在不同程度的纤维化及间质胶原增生和糖原沉积.结论 高频起搏左心耳8周建立的慢性AF模型,心肌超微结构、心房构型和心功能发生明显改变,引起心房结构重构和收缩功能重构,这是发生心房颤动的重要原因之一.     

MRI评价螺内酯对急性心肌梗死患者心室重构的影响

目的探讨应用小剂量螺内酯干预急性心肌梗死（AMI）患者左室重构（LVRM）的影响。方法80例AMI患者,采用随机、对照方法,分为对照组（n=38）常规治疗,螺内酯组（n=42）在常规治疗的基础上加用螺内酯40mg/d。在治疗6个月内检测2组患者血清Ⅲ型前胶原氨基端肽（PⅢNP）、血清透明质酸（HA）及心脏核磁共振,以评价左室纤维化和左室功能。结果治疗6个月后,螺内酯组PⅢNP、HA较对照组明显下降（P〈0.01）,左室收缩末期内径与对照组相比明显下降,LVEF明显升高,延迟强化灶体积明显下降（P〈0.05）。结论常规治疗的基础上联合应用小剂量螺内酯,可进一步抑制左室重构、改善心功能。     

犬阵发性房颤转复窦律后时间依赖性心房电逆重构的研究

目的 探讨犬阵发性房颤转复期间时间依赖性心房电逆重构情况.方法 健康成年杂种犬18只,随机分为快速起搏组(n=10,ATP组)和假手术组(n=8,Sham组).分别于快速右心房起搏48 h及转复24 h期间,在0、48(起搏停止)、52、56、60、64,68、72 h电生理检测高右房(HRA)的有效不应期(ERP)、传导速度(CV)、折返波长(WL)、频率自适应性、房颤诱发率等反映心房电生理特性的指标.结果 起博48 h后,ATP组ERP、CV、WL较Sham组减少,ATP组频率自适应性较Sham组降低(P<0.05),房颤诱发率明显增加.停止起搏24 h后ERP、FA、房颤诱发率与Sham组及起搏前相比差异无统计学意义(P>0.05);CV与Sham组及起搏前相比差异有统计学意义(P<0.05).结论 犬48 h快速心房起搏所致左、右心房电重构在转复24 h后,ERP、FA、房颤诱发率发生逆转,但CV、WL仍不能逆转.     

犬24 h房颤心房形态及心功能变化的研究

目的:探讨心房颤动(AF)持续24 h对犬左、右房大小及心功能的影响。方法:全麻状态下,快速起搏(600次/min)犬右心房建立房颤模型,观察AF后0、4、8、12、24 h左、右心房横径、心室射血分数(EF)的变化。结果:随着AF的持续,左、右房横径均逐渐增大,但增大幅度与0 h比较差异无统计学意义(P>0.05)。房颤12 h心室射血分数降低7.48%,24 h降低8.81%,与0 h比较差异有统计学意义(P<0.05)。结论:快速起搏犬右心房所致AF持续24 h后,心室射血分数从12 h开始降低,与心房肌降低泵血功能,减少向心室排血有关,是心房增大的原因之一。心房结构随着AF进程有逐渐增大的趋势,可能参与了阵发性房颤的结构重构。     

氧化应激对心房颤动犬心房病理组织学及超微结构改变的影响

目的 观察氧化应激对慢性心房快速起搏诱发心房颤动(房颤)犬心房肌钙激活蛋白酶Ⅰ表达及肌细胞超微结构改变的影响.方法 20只犬无菌条件下开胸手术,植入高频起搏器(400次/分),建立房颤犬模型,分为假手术组(不起搏),对照组和普罗布考组心房快速起搏6周.普罗布考组于起搏前1周服用普罗布考(100 mg/kg),至起搏6周结束.采用免疫组化方法和Western印迹法检测各组犬心房肌钙激活蛋白表达情况;分别于起搏前和起搏6周后,记录各组犬房颤诱发情况;比色法检测各组犬心房肌氧化应激相关指标.结果 对照组左、右心房肌肌溶解比率[(53.6±11.8)%,(58.5±9.2)%]比假手术组[(4.4±3.1)%,(4.1±2.9)%]显著增加(P＜0.01);对照组比假手术组心房肌细胞线粒体肿胀伴糖原沉积明显,心房肌钙激活蛋白酶Ⅰ表达显著上调(P＜0.01);普罗布考组左、右心房肌细胞病理组织学和超微结构改变比对照组明显减轻,肌溶解比率明显减少[(12.3±3.2)%,(12.0±2.6)%,P＜0.01],钙激活蛋白酶Ⅰ表达显著下调(P＜0.01).普罗布考组心房肌MDA水平比对照组显著降低(P＜0.01),T-AOC和抗O2-水平明显增加(P＜0.01),房颤诱发率和平均持续时间显著减少(均P＜0.01).心房肌钙激活蛋白酶Ⅰ表达和MDA均与肌溶解程度呈显著正相关(r=0.958,r=0.939,P＜0.01).结论 普罗布考能够通过抑制氧化应激,抑制房颤犬心房肌肌溶解等病理组织学和超微结构变化,防止心房颤动犬心房重构,减少房颤发生.     

羊持续心房颤动心房有效不应期变化的时间进程及其逆转观察

目的：探讨持续心房颤动（AF）心房有效不应期（ERP）变化的时间进程及其逆转过程.方法：采用起搏方法建立AF模型,在起搏前和起搏后的第1 d,3 d,5 d,7 d对左、右心耳的有效不应期（ERP）进行测定.采用S1S2程序刺激,基础起搏周长（PCL）分别为400 ms,350 ms,300 ms,250 ms,200 ms,S2为200 ms,以5 ms的步长递减.程序刺激结合Burst刺激对上述心房结构进行AF的诱发,记录AF的发生频率.上述相同方法对起搏停止后0 h,3h,5 h,24 h左、右心耳的ERP进行测定.结果：各个基础起搏周长下左、右心耳的ERP在AF后1 d,3 d,5 d,7 d逐渐缩短,且较AF前明显缩短（P＜0.05）;AF终止后左、右心耳的ERP逐渐延长,但AF终止0 h,3 h,5 h ERP与AF前相比仍有明显缩短（P＜0.05）;AF终止后24 h ERP基本恢复到AF前水平,两者相比差异无统计学意义（P＞0.05）;随着AF持续时间的延长,左、右心耳AF的诱发率逐渐增高,与AF前相比,AF后1 d、3 d、5 d、7 d AF的诱发率明显增高（P＜0.05）.结论：随着AF持续,心房的ERP逐渐缩短,AF的诱发率逐渐增高,AF终止后缩短的ERP逐渐延长致AF前水平.     

快速起搏对家兔心房肌钙通道表达的影响及螺内酯干预的研究

目的观察螺内酯对快速心房起搏对家兔心房肌细胞L型钙离子通道亚基表达的影响。方法家兔18只随机分为3组,对照组、起搏组及螺内酯组各6只。起搏组和螺内酯组经颈内静脉将电极植入右心房,以600次/min行快速心房起搏8 h,起搏后应用半定量反转录-聚合酶链反应检测心房肌钙离子通道α1C亚基及β1亚基mRNA的表达。结果与对照组比较,起搏组钙离子通道α1C亚基及β1亚基mRNA表达明显减少,分别下降22%和26%,差异有统计学意义(P<0.01);螺内酯组钙离子通道α1C亚基及β1亚基mRNA表达降低明显减少,分别下降13%和17%,与起搏组相比,有统计学意义(P<0.05)。结论螺内酯可预防快速起搏后钙离子通道表达亚基的降低。     

Changes in microRNAs expression are involved in age-related atrial structural remodeling and atrial fibrillation

Background Small noncoding microRNAs regulate gene expression in cardiac development and disease and have been implicated in the aging process and in the regulation of extracellular matrix proteins.However,their role in age-related cardiac remodeling and atrial fibrillation (AF) was not well understood.The present study was designed to decipher molecular mechanisms underlying age-related atrial structural remodeling and AF.Methods Three groups of dogs were studied:adult and aged dogs in sinus rhythm and with persistent AF induced by rapid atrial pacing.The expressions of microRNAs were measured by quantitative real-time polymerase chain reaction.Pathohistological and ultrastructural changes were tested by light and electron microscopy.Apoptosis index of myocytes was detected by TUNEL.Results Samples of atrial tissue showed the abnormal pathohistological and ultrastructural changes,the accelerated fibrosis,and apoptosis with aging and/or in AF dogs.Compared to the adult group,the expressions of microRNAs-21 and -29 were significantly increased,whereas the expressions of microRNAs-1 and-133 showed obvious downregulation tendency in the aged group.Compared to the aged group,the expressions of microRNAs-1,-21,and-29 was significantly increased in the old group in AF; contrastingly,the expressions of microRNA-133 showed obvious downregulation tendency.Conclusion These multiple aberrantly expressed microRNAs may be responsible for modulating the transition from adaptation to pathological atrial remodeling with aging and/or in AF.     

卡托普利对心动过速心肌病心肌缝隙连接蛋白重构的影响

目的研究卡托普利对心动过速心肌病（tachycardia induced cardiomyopathy, TIC）实验犬心室肌中缝隙连接蛋白重构的影响。方法24只犬随机分为3组。起搏组：实验犬植入永久起搏器，经颈外静脉途径将起搏电极导线置入右心耳(起搏频率350～450次／min)。起搏加药物组：起搏器植入同起搏组，起搏器植入前3?d至起搏8周后，每日给予卡托普利50mg 2次／日口服；对照组：实验犬未植入起搏器也未服药。分别在起搏前及起搏后第1、4、8周记录12导联心电图并行超声心动图检查，起搏8周后行心导管检查，并用激光共聚焦显微镜测定3组左心室肌缝隙连接蛋白（Connexin43, Cx43）含量。结果左心室肌Cx43含量比较：起搏组vs对照组（P＜0.001）；起搏组vs起搏加药物组（P＜0.05），起搏组Cx43含量均明显减低。结论卡托普利有明显延缓慢性实验犬TIC左心室Cx43下降的趋势。