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.     

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.     

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。     

心房颤动电生理重构的实验研究

目的 :研究心房颤动 (atrialfibrillation ,AF)时心房肌的电生理重构。方法 :快速持续起搏犬右心房 8～ 10周 ,制备持续性AF模型。比较对照犬 ( 8只 )与起搏犬 ( 10只 )的有效不应期 (effectiverefractoryperiod ,ERP)和心房颤动波周长 (atrialfibrillationcyclelength ,AFCL)的变化来分析心房肌的电生理重构。结果 :起搏组P波时间和PA间期比起搏前明显延长 (P波时间 90 5± 10 5对 5 3 6± 8 3ms ;PA间期 5 9 6± 8 8对 3 8 6± 11 4ms ,P <0 0 5 )。经程序刺激ERP较对照组明显缩短 (S1S13 0 0ms 115± 2 3对 15 0± 2 1;S1S14 0 0ms 10 5± 2 7对 15 4± 2 4ms ,P <0 0 5 )。同一心房不同部位的ERP和AFCL也存在差异。结论 :心房率的长期变化可引起ERP和AFCL的变化 ,即心房肌发生电生理重构 ,而且不同部位心房肌电生理重构是不同的。     

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?     

Calpain I inhibition prevents atrial structural remodeling in a canine model with atrial fibrillation

Background Atrial fibrillation （AF） is accompanied by atrial structural remodeling. Calpain activity is induced during AE To test a causal relationship between calpain activation and atrial structural changes, N-acetyI-Leu-Leu-Met （ALLM）, a calpain inhibitor, was utilized in a canine AF model. Methods Fifteen dogs were randomly divided into 3 groups： sham-operated group, control group and calpain inhibitor group; each with 5 dogs. Sustained AF was induced by rapid right atrium pacing at 600 beats per minute for 3 weeks. ALLM was administered at a dosage of 1.0 mg-kg-l-d1 in the calpain inhibitor group. Three weeks later, the proteolysis, protein expression of TnT and myosin, calpain I localization and expression and structural changes were examined in left atrial free walls, right atrial free walls and the interatrial septum respectively. Atrial size and contractile function were also measured by echocardiography. Results Long-term rapid atrial pacing induced marked structural changes such as enlarged atrial volume, myolysis, degradation of TnT and myosin, accumulation of glycogen and changes in mitochondrial shape and size, which were paralleled by an increase in calpain activity. The positive correlation between calpain activity and the degree of myolysis （rs=0.90 961, P〈0.0001） was demonstrated. In addition to structural abnormalities, pacing-induced atrial contractile dysfunction was observed in this study. The pacing-induced atrial structural alterations and loss of contractility were partially prevented by the calpain inhibitor ALLM. Conclusions Activation of calpain represents key features in the progression towards overt structural remodeling. Calpain inhibitor, ALLM, suppressed the increased calpain activity and reversed structural remodeling caused by sustained atrial fibrillation in the present model. Calpain inhibition may therefore provide a possibility for therapeutic intervention in AE     

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…     

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.     

Effects of spironolactone on electrical and structural remodeling of atrium in congestive heart failure dogs

Background Renin-angiotensin-aldosterone system has been demonstrated to be associated with both congestive heart failure （CHF） and atrial fibrillation （AF）. This study investigated the effects of spironolactone, a kind of aldosterone antagonist, on atrial electrical remodeling and fibrosis in CHF dogs induced by chronic rapid ventricular pacing. Methods Twenty one dogs were randomly divided into sham-operated group, control group, and spironolactone group. In control group and spironolactone group, dogs were ventricular paced at 220 beats per minute for 6 weeks. Additionally, spironolactone at 15 mg.kgl.d1 was given to dogs 1 week before rapid ventricular pacing until pacing stopped. Transthoracic and transoesophageal echocardiographic examinations were performed to detect structural and functional changes of the atrium. Swan2 Ganz floating catheters were used to measure hemadynamics variances. Atrial effective refractory period （AERP）, AERP dispersion （AERPd） conduction velocity （CV） were determined. The inducib atrial fibrosis was quantified with Masson staining. intra- and inter-atrium conduction time （CT） and intra-atrium ity and duration of AF were also measured in all groups. Finally, Results AERP did not change significantly after dogs were ventricular paced for 6 weeks. However, AERPd, intra- and inter-atrium CT increased significantly, and CV decreased apparently, which was negatively correlated to the atrial fibrosis （r=-0.74, P〈0.05）. Simultaneously, left atriums were enlarged and cardiac hemadynamics worsened in pacing dogs. Although spironolactone could not affect cardiac hemadynamics effectively, it can obviously improve left atrial ejection fraction （P〈0.05）. Spironolactone treatment did not alter AERP duration, but this medicine dramatically decreased AERPd （P〈0.05）, shortened intra- and inter-atrium conduction time （P〈0.05）, and increased atrium CV. Moreover, spironolactone decreased the inducibility and duration of AF （P〈0.05）, as well as at     

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.     

白藜芦醇干预对慢性心房纤颤猪心房组织中去乙酰化酶1表达的影响

目的探讨白藜芦醇（resveratrol,RES）干预对快速右房起搏诱发的慢性心房纤颤（atrial fibrillation,AF）猪心房组织中去乙酰化酶（SIRT）1表达的影响。方法18头小家猪（雌雄不拘）随机分为3组（n=6）：起搏组（ATP组）、假手术组（sham组）和白藜芦醇干预组（RES组）。采用Seldinger血管穿刺技术穿刺右或左侧颈内静脉送入双极电极至右心房并连接至实验用起搏器（AOO）,快速起搏心房（500次/min）2周（假手术组猪不起搏）制备慢性AF实验模型。RES组猪于起搏前1周开始服用RES（2.5 mg.kg-1.d-1）。RT-PCR分析SIRT1mRNA表达情况,Western blot法检测SIRT1蛋白表达水平的变化。结果RES组SIRT1 mRNA和蛋白的表达较ATP组和sham组均明显增加（P〈0.05）,ATP组稍高于sham组但差异无统计学意义（P〉0.05）。结论RES干预可以明显增强快速起搏右房诱发的慢性AF猪心房组织中SIRT1的表达。     

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&lt;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&lt;0.05). However, Diltiazem could not prevent the increase of AERP dispersion at 3 hours (P&lt;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.     

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。     

High mobility group box 1 protein: possible pathogenic link to atrial fibrillation

Atrial fibrillation (AF) is the most common sustained dysrhythmia in clinical practice. The bulk of evidence suggests that inflammatory processes, oxidative stress and matrix metalloproteinase are associated with development of AF. However, these agents may be involved in high mobility group box 1 protein (HMGB1). We hypothesized that HMGB1 may be a possible pathogenic link to AF. A growing body of evidence supports these hypotheses. First, the level of serum HMGB1 is significantly increased in patients with AF including paroxysmal and persistent AF. Second, HMGB1 has been identified as a new pro-inflammatory cytokine in cardiovascular diseases, along with tumor necrosis factor (TNF)-α, interleukin (IL)-6, and C-reactive protein, and there is cross-talk between HMGB1 and inflammatory cytokines. Third, oxidative stress is involved in the release of the pro-inflammatory cytokine, HMGB1, indicating there is cross-talk between oxidative stress and inflammation, and oxidative stress may reinforce the effect of inflammation on the pathogenesis of AF and inflammation may play a more important role in the pathogenesis of AF. Fourth, HMGB1 can promote matrix metalloproteinase-9 upregulation and activation. Fifth, HMGB1 receptors (receptor for advanced glycation end products, Toll-like receptor-2,4) may mediate the atrial structural remodeling or be up-regulated in patients with non-valvular AF. These results suggest that HMGB1 may participate in the pathogenesis of AF and provide a potential target for pharmacological interruption of AF.     

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.     

交感神经在心房颤动中的作用

交感神经在房颤的发生及维持中起了重要作用。交感神经使多种离子通道电流发生改变,缩短心房有效不应期,升高心房有效不应期离散度,诱发心房颤动。但目前,各种离子通道电流在房颤机制中的作用尚未完全研究清楚。房颤导致交感神经重构,使交感神经在心房的分布密度增加且分布不均一,这进一步使房颤得以维持。     

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。     

心房颤动犬心房肌细胞骨架重构及贝那普利的干预作用

目的 观察快速心房起搏心房颤动(房颤)犬心房肌细胞骨架重构及贝那普利的干预作用.方法 采用慢件快速左心房起搏建立房颤犬模型,分为假手术组(6只)、房颤组(7只)、干预组(6只).房颤组应用固定频率型起搏器,600次/min起搏6周;干预组于起搏前1周开始每日服贝那普利(1 mg/kg).实验结束时取材,HE染色测定心房肌细胞直径;Masson染色进行心房肌纤维化定量分析;免疫组织化学法检测结蛋白心脏原位蛋白分布及表达;RT-PCR方法测定心房肌组织β-微管蛋白、结蛋白mRNA表达水平.结果 假手术组、房颤组、干预组左心房肌细胞直径分别为(19.6 ±2.9)μm、(27.9 ±3.8)μm、(25.1 ±3.4)μm,右心房分别为(18.7 ±2.6)μm、(26.8 ±3.2)μm、(25.2 ±3.5)μm,房颤组、干预组左、右心房肌细胞直径均明显长于假手术组(均P＜0.01);左心房胶原容积分数(CVF)分别为(9.2±0.9)%、(16.9 ±1.1)%、(11.3 ±0.8)%,右心房CVF分别为(9.3±0.8)%、(15.7 ±2.3)%、(10.9 ±0.8)%,房颤组左、右心房CVF均高于假手术组(均P＜0.01),干预组均明显低于房颤组(均P＜O.01).免疫组化示房颤组结蛋自在细胞质内表达增多,而闰盘处表达不明显,房颤组左、右心房肌结蛋白吸光度值均高于假手术组(均P＜0.01),干预组均明显低于房颤组(均P＜0.01).房颤组左、右心房肌结蛋白、微管蛋白mRNA表达均高于假手术组(均P＜0.01);干预组房颤组(均P＜0.01).结论 快速心房起搏房颤犬心房肌细胞骨架发生重构且贝那普利对其有干预作用.     

Association of prolidase activity, oxidative parameters, and presence of atrial fibrillation in patients with mitral stenosis

BACKGROUND: Mitral stenosis (MS) is a common cause of atrial fibrillation (AF). Oxidative stress and inflammation factors were shown to be involved in atrial remodeling. The study aim was to compare the oxidative parameters and prolidase activity in severe MS patients with and without AF. METHODS: The study population was comprised of 33 patients with MS and sinus rhythm (group I), 27 patients with MS and AF (group II), and 25 healthy controls (group III). Plasma prolidase activity, total antioxidant capacity (TAC), total oxidative status (TOS), and oxidative stress index (OSI) were determined. Additionally, we measured tissue TOS and TAC in patients with mitral valve replacement. RESULTS: TAC and OSI were higher, but TOS and prolidase were lower in patients with MS than control (all p <0.001). These parameters were similar in group I and group II (ANOVA p >0.05). Tissue TAC was significantly lower in group II than group I (0.015 +/- 0.01 vs. 0.026 +/- 0.01 mmol Trolox equiv/L, p = 0.014), tissue TOS was similar between groups I and II (0.24 +/- 0.06 vs. 0.22 +/- 0.05 mmol Trolox equiv/L, p = 0.161). Presence of AF was correlated with systolic blood pressure, left atrial diameter, plasma TAC, tissue TAC, plasma TOS, plasma OSI, and plasma prolidase activity. Tissue TAC level (beta = -0.435, p = 0.006) and left atrial diameter (beta = 0.460, p = 0.003) were independently related with presence of AF in patients with MS. CONCLUSIONS: This study suggested that the presence of AF in patients with severe MS may be associated with the plasma prolidase activity, tissue and plasma oxidative parameters.     

犬心房与肺静脉交感神经分布与阵发性心房颤动的关系

目的 探讨犬交感神经末梢在心房与肺静脉分布的特点及其与房颤诱发的相关性.方法 16只健康杂种犬,全麻、左右侧开胸.刺激双侧迷走交感干,分别于右心耳、左心耳、左心房及四支肺静脉行S1S1猝发刺激及S1S2程序刺激,观察心房及肺静脉不同部位房颤的诱发率.随后,处死动物,行心房、肺静脉交感神经抗酪氨酸羟化酶(TH)抗体染色,计算心房及肺静脉各部位交感神经密度,比较交感神经密度与房颤诱发之间的关系.结果 14只犬完成全部试验.除右下肺静脉房颤诱发率较低外,余各部位房颤诱发率无明显差异;心房和心耳TH染色阳性的神经密度分别为高于肺静脉内的神经密度[(128±65)/mm2,(76±29)/mm2,P=0.02];能诱发房颤的犬的TH染色阳性的神经密度高于未能诱发房颤(P＞0.05).结论 心房、心耳的交感神经分布比肺静脉的交感神经分布的密度大;房颤诱发与心房和肺静脉内交感神经分布的密度有一定关系.