选择性刺激犬房室结脂肪垫的电生理实验研究

目的 选择性刺激犬心脏房室结(AVN)脂肪垫,观察其对心脏窦房结(sAN)功能及房颤(AF)时房室传导的影响.方法 取蒙古犬36只,经开胸直接刺激AVN脂肪垫.刺激能量由O mA逐级增高直至AF诱发.测量不同能量状态下窦性周期长度(SCL)及AF诱发阈值.AF诱发后,继续逐级增加刺激电流及脉宽,分别记录诱发AF的连续lO个RR间期.结果 AF诱发阈值为(4.1±1.2)mA.无1例犬(0%)在直接AVN脂肪垫刺激下延长SCL>10%.逐级递增的AVN脂肪垫刺激导致AF的RR间期进行性延长.结论 直接AVN脂肪垫刺激诱发AF并有效延长AF时的房室传导,通过介入方法 定向消融AVN脂肪垫有望成为有效控制AF心室率的新方法 .     

通过刺激自主神经结丛建立持续局灶性心房颤动动物模型

目的探讨一种通过刺激自主神经结丛来建立持续局灶性心房颤动(房颤)动物模型的新方法。方法共选取20只雄性杂交狗,随机分为乙酰胆碱(Acetylcholine)组(10只)和卡巴胆碱(Carbachol)组(10只)。用苯巴比妥钠麻醉,行右侧开胸及心包切开手术,暴露出右肺静脉与右心房之间的脂肪垫,将一注射针插入该脂肪垫中,以备注入乙酰胆碱或卡巴胆碱。将多电极导管(CordisWebster公司,美国)缝合在右上肺静脉、右心房、左心房上。分别在给药前后(乙酰胆碱组:10 mmol/L乙酰胆碱0.5 mL;卡巴胆碱组:10 mmol/L卡巴胆碱0.5 mL),于右心房处行程序期前刺激,来测定有效不应期及诱发房颤,刺激强度分别采用2倍、4倍、10倍及20倍起搏域值,如出现房颤,则记录房颤持续最长时间及房颤时心房电活动的平均周期。结果向右心房脂肪垫注射乙酰胆碱或卡巴胆碱后可明显缩短心房有效不应期,增加诱发房颤最大与最小偶联间期之差,延长房颤持续的时间,缩短房颤时心房电活动的平均周期。乙酰胆碱组,未注射乙酰胆碱时,在刺激强度为2倍、4倍、10倍及20倍起搏域值时,在右心房处所测心房有效不应期分别为(116.3±17.8)ms,(102.3±22.7)ms,(91.7±21.9)ms和(80.0±23.0)ms,注入乙酰胆碱后则分别缩短为(103.8±26.1)ms(P>0.05),(94.7±21.9)ms(P<0.05),(74.3±20.0)ms(P<0.01)和(65.5±17.8)ms(P<0.05)。未注射乙酰胆碱或卡巴胆碱时,所诱发房颤均为短阵性房颤,持续时间为(9.7±6.0)s(乙酰胆碱组)和(10.4±8.0)s(卡巴胆碱组),心房平均电活动周期为(122.0±9.0)ms(乙酰胆碱组)和(120.0±8.0)ms(卡巴胆碱组);注入乙酰胆碱后持续时间延长为(596.7±281.0)s(P<0.01),心房平均电活动周期缩短为(76.0±32.0)ms(P<0.05);注入卡巴胆碱后则诱发出频率极快、持续时间更长的房颤,持续时间延长为(2 364.0±1169.0)s(P<0.01),心房平均电活动周期缩短为(39.0±12.0)ms(P<0.01)。结论向狗右心房脂肪垫注射卡巴胆碱可成功建立持续性房颤的动物模型。     

氯沙坦对家兔房颤的电生理研究

目的探讨氯沙坦对家兔快速心房起搏所致房颤(AF)的预防作用。方法28只新西兰大耳白兔,随机分为氯沙坦组和对照组,前者灌胃法喂以氯沙坦15mg·kg-1·d-1,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,心房快速起搏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[(16.43±5.56)ms和(30.71±8.86)ms,P<0.01]。②AF的诱发率,氯沙坦组少于对照组(4/14和12/14,P=0.006)。③AF发作的持续时间,氯沙坦组短于对照组[(47.5±9.6)s和(115.0±8.0)s,P<0.001]。④AFCL,氯沙坦组长于对照组[(85.0±10.0)ms和(45.0±8.0)ms,P<0.001]。结论氯沙坦可有效预防兔快速心房起搏所致AF的发生。     

快速心房电刺激对人心房不应期的影响及卡托普利的干预作用

探讨快速心房电刺激对人心房有效不应期 (AERP)的影响及卡托普利的干预作用。选择本院行射频消融术的 38例成年患者为研究对象 ,随机分为卡托普利组 (14例 )、维拉帕米组 (12例 )及生理盐水对照组 (12例 )。分别在阻断心脏自主神经后 ,观察各组用药前、后及快速心房刺激后AERP的变化及AF诱发情况。结果 :①快速心房刺激可使 5 7.9%成人正常心脏诱发AF ;②诱发AF后AERP明显缩短 ,而未诱发AF者的AERP无明显变化 ;③卡托普利及维拉帕米均能显著延长诱发AF患者的AERP ;④卡托普利能减少AF诱发率 ,并缩短AF持续时间 ;而维拉帕米则使AF诱发率增加、持续时间延长。结论 :①快速心房刺激可使部分患者AERP缩短 ,并诱发这类患者发生AF ;②卡托普利可显著延长诱发AF患者的AERP ,并使AF诱发率降低、持续时间缩短     

射频消融第三脂肪垫对犬心房电生理参数及心房颤动诱发的影响

目的研究射频消融第三脂肪垫对犬心房电生理参数及心房颤动(房颤)诱发的影响。方法观察12只杂种犬在不同起搏周长下,消融第三脂肪垫前后心房不同部位有效不应期(AERP)、AERP离散度、AERP频率适应性,房颤诱发率及其诱发窗口的变化。结果与消融前相比,消融后心率变化差异无统计学意义(P>0.05)。随着起搏周长变短,AERP明显缩短,且差异具有统计学意义(均为P<0.05)。消融术后高位左心房、低位左心房、左心耳部位AERP明显缩短,高位右心房、低位右心房、右心耳部位AERP明显延长(均为P<0.05)。AERP离散度差异无统计学意义(P>0.05)。消融后不同测量部位的房颤诱发率均降低及房颤诱发窗口增宽。结论消融第三脂肪垫达到部分去迷走神经化,使左心房AERP缩短,同时使房颤诱发率降低及房颤诱发窗口增宽。     

心房肌易损性与阵发性心房颤动的发生机制

目的探讨左、右心房肌复极,及其易损性与阵发性心房颤动(AF)的发生与维持机制。方法应用单相动作电位(MAP)技术记录14只犬左、右心房肌的复极达90%动作电位时程(APD90),通过S1S2程序刺激,同时记录心房有效不应期(ERP)及相对不应期(RRP),观察反复心房激动(RAF,在S1S2的早搏刺激后,发生2个以上的连续心房活动,从心房刺激到RAF第一个激动的间期必须小于250 ms)及AF的诱发。结果14只犬S1S2间期递减至130±32 ms时,可出现RAF,随后当S1S2间期缩短为110±28 ms时AF发作。AF发作前大多数可记录到RAF(66.7%);共诱发出15阵RAF,左房11阵,右房4阵,左房RAF的发生率明显多于右房(P<0.05);共诱发出18阵AF,左房诱发出12阵,右房诱发出6阵。左房的AF诱发率明显多于右房(P<0.05)。结论AF发作前多伴有RAF发作;RAF是易发生阵发性AF的特征性表现,代表心房的易损性;左右心房易损性不同。     

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。     

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。     

刺激左右颈部迷走交感干对兔心房电生理特性的影响

目的:探讨心脏外在自主神经对心房电生理特性的影响及其在房性心律失常发生中的可能作用。方法:新西兰大白兔10只静脉麻醉后,经右侧颈静脉将6F电极导管置入右心房,并给予设定的电程序刺激,记录心房有效不应期(AERP)、P波离散度(PD)、发生心房纤颤(AF)动物的比例数及心房易损窗口(WOV),再分别给予左右单侧及双侧颈迷走交感干(CVST)电刺激,使心率(HR)较基础状态分别减慢10%、30%和50%,重复上述电刺激,并测量上述电生理指标。将10只新西兰大白兔颈部迷走交感干刺激前后所测指标先后对照。结果:随着刺激CVST强度的增加,与基础状态相比较,AERP逐渐缩短,至刺激强度使HR减慢10%(双侧)、30%(右侧)和50%(左侧)时,AERP缩短具有统计学意义(P0.05);PD随刺激强度的增加呈逐渐增大的趋势,至刺激强度使HR减慢30%(右侧、双侧)、50%(左侧)时,与基础状态相比PD明显增大(P0.05)。以上两个指标随着刺激强度的增加,变化均更显著(P0.01)。无论给予实验设定的任何强度的左、右单侧或是双侧CVST刺激,发生AF的动物的比例数均有增多的趋势,但无统计学意义;仅在进行双侧CVST刺激并当强度达到使HR较基础减慢50%时,WOV增宽才具有统计学意义[(7.6±3.5)msvs.(3.4±1.5)ms,P0.05]。结论:右心房的电生理特性受双侧CVST的影响,且以右侧为优势,其中左右CVST对右心房电生理特性的影响存在叠加作用。     

外源性与内源性自主神经刺激对心房颤动诱发性的影响

目的探讨心脏外源性与内源性自主神经刺激对心房颤动(房颤)诱发性的影响。方法16只成年犬静脉麻醉后,分离右颈迷走神经干(VST);再行右侧开胸手术,暴露靠近右上肺静脉的心脏脂肪垫(内含心脏自主神经丛,即GP),将1根电极导管固定贴靠于右上肺静脉,使其头端电极贴靠右上肺静脉与左房交界处,进行程序期前刺激,采用2倍、4倍、10倍阈值的刺激强度进行基础程序期前刺激(control),并测量相应的心房不应期(ARP)及房颤诱发窗宽(WOV);再分别加用VST刺激或GP刺激,测量在相应刺激条件下程序期前刺激所获得的ARP及WOV。结果平均基础心率(HR)为153±22次/min,VST刺激下HR为79±44次/min,GP刺激下HR为87±99次/min(后二者比较,P>0·05)。最短的ARP在control状态下为101±20ms、VST刺激下为90±17ms、GP刺激下为91±13ms,VST刺激下及GP刺激下均较control明显缩短(P<0·05),VST刺激下与GP刺激下的差异无统计学意义(P>0·05)。三者的累计WOV分别为control22±34ms、VST刺激下44±45ms、GP刺激下99±75ms,三者间每两者的差异均有统计学意义(P<0·05)。结论在降低心率相近的情况下,电刺激心脏内源性自主神经丛与电刺激心脏外源性自主神经引起的不应期缩短相近,但前者更容易诱发房颤。     

Vagal denervation and atrial fibrillation inducibility: Epicardial fat pad ablation does not have long-term effects

BACKGROUND: Major epicardial fat pads contain cardiac ganglionated plexi of the autonomic, predominantly vagal nerves. Vagal denervation may improve the success rate of atrial fibrillation (AF) treatment. OBJECTIVES: The purpose of this study was to elucidate the long-term effects of fat pad ablation on the electrophysiologic characteristics of the atrium and AF inducibility. METHODS: Six mongrel dogs were studied. Cervical vagal stimulation was applied to determine effects on the sinus node, AV node, atrial effective refractory period (AERP), and AF inducibility. AERP and AF inducibility were evaluated at both the right atrial and left atrial appendages and at the right atrial and left atrial free walls. Radiofrequency energy was delivered epicardially to the entire areas of two major fat pads: right pulmonary vein fat pad and inferior vena cava-left atrium fat pad. Cervical vagal stimulation then was applied to confirm the acute effects of fat pad ablation. The same evaluation was repeated 4 weeks later. RESULTS: The effects of vagal stimulation on the sinus node, AV node, and AERP were significantly eliminated immediately after fat pad ablation. However, these denervation effects disappeared after 4 weeks. At baseline, AF inducibility was increased by vagal stimulation (right atrial appendage: 72% +/- 31% vs 4.8% +/- 12%; right atrial free wall: 75% +/- 31% vs 0.0% +/- 0.0%; left atrial appendage: 60% +/- 29% vs 0.0% +/- 0.0%; left atrial free wall: 65% +/- 42% vs 0.0% +/- 0.0%). Fat pad ablation significantly reduced this vagal stimulation effect (8.3% +/- 20%, 10% +/- 22%, 17% +/- 29%, and 25% +/- 29%, respectively). However, similar to baseline, AF inducibility was strongly augmented by vagal stimulation 4 weeks after fat pad ablation (96% +/- 10%, 100% +/- 0.0%, 100% +/- 0.0%, and 95% +/- 11%, respectively). CONCLUSION: Radiofrequency fat pad ablation may not achieve long-term suppression of AF induction in this canine model.     

Long-term changes in sequence of atrial activation and refractory periods: no evidence for "atrial memory".

OBJECTIVES: The purpose of this study was to test whether the spatial distribution of the atrial refractory period (AERP) and the vulnerability to atrial fibrillation (AF) are altered by long-term changes in the sequence of atrial activation. BACKGROUND: The spatial distribution of the AERP plays an important role in AF. Changes in the activation sequence have been postulated to modulate atrial repolarization ("atrial memory"). METHODS: Six goats were chronically instrumented with epicardial atrial electrodes to determine activation time and AERP at 11 different areas of the right (RA) and left (LA) atrium and the Bachmann bundle. Activation time and AERP were measured during sinus rhythm and during prolonged RA and LA pacing (1 week RA pacing, 2 weeks LA pacing, 1 week RA pacing; 150 bpm). Inducibility of AF was determined by the number of atrial sites where single premature stimuli induced AF paroxysms >1 second. RESULTS: During sinus rhythm (106 +/- 4 bpm), AERP was longest at the Bachmann bundle and shortest at the LA free wall (185 +/- 6 ms and 141 +/- 5 ms, P < .001). In five of six goats, an inverse correlation between local activation time and AERP was found during sinus rhythm (r = -0.53 +/- 0.05; P < .05). The increase in atrial rate during RA and LA pacing caused an overall shortening of AERP from 167 +/- 6 ms to 140 +/- 6 ms (P < .001). However, a switch between long-term RA and LA pacing did not significantly change AERP at any of the 11 atrial regions and had no significant effect on AF inducibility. CONCLUSIONS: During sinus rhythm, an inverse relationship exists between the sequence of atrial activation and the local refractory period. However, long-term changes in the sequence of atrial activation do not alter the spatial distribution of AERP or the inducibility of AF.     

窦房结脂肪垫对犬右上肺静脉电生理特性影响的研究

目的研究不同水平刺激窦房结脂肪垫(SANFP)对右房(RA)及右上肺静脉(RSPV)的有效不应期(ERP)及心房颤动(简称房颤)诱发率的影响,探讨SANFP对房颤发生维持的作用。方法6只犬麻醉后经右侧开胸暴露RSPV及SANFP,以0.6～2,5,8mV三种不同电压强度水平、60ms频率刺激SANFP,同时以S1S2刺激观察三种水平下RA游离壁远、中、近端及RSPV远、中、近端ERP的变化;同样方法刺激SANFP以S1S1和S1S2程序刺激诱发房颤,测定房颤的诱发率。结果以5mV电压刺激窦房结脂肪垫RSPV近端ERP较基础时明显缩短(90±24msvs109±16ms,P<0.05),其房颤诱发率50%;以5,8mV电压刺激SANFP时RA游离壁近端、中端ERP变化较基础时明显缩短(96±20msvs117±14ms,65±20msvs117±14ms,P均<0.05),其房颤诱发率100%。结论窦房结脂肪垫可能在肺静脉起源的房颤的诱发和维持中起了重要作用。     

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.     

序列消融犬窦房结脂肪垫和房室结脂肪垫对迷走神经介导心房颤动诱发的影响

目的 研究旨在探索序列消融窭房结脂肪垫(sinus atrial node fat pad,SANFP)和房室结脂肪垫(atrialventricular node fat pad,AVNFP)对迷走神经介导的心房颤动(房颤)诱发的影响.方法 18只健康成年家犬分为二组,每组9只.A组优先消融SANFP,再联合消融SANFP+ AVNFP;B组优先消融AVNFP,再联合消融SANFP+ AVNFP.高频电刺激左、右侧迷走神经干制作迷走神经介导的房颤模型,测定消融前、后的房颤诱发率及心房和肺静脉不同部位有效不应期(effective refractory period,ERP).结果 (1)迷走神经干刺激可显著增加房颤的诱发率,且右侧迷走神经干刺激下的房颤诱发率高于左侧迷走神经干[(60.0±0.0)％比(18.4±22.1)％].(2)优先消融SANFP可显著降低左侧迷走神经干或右侧迷走神经干刺激下房颤的诱发率(分别降低了67.0％和72.0％),联合消融SANFP+ AVNFP可进一步降低2V电压的左侧迷走神经干或右侧迷走神经干刺激下房颤的诱发率(分别较消融前降低了100％和95.5％).而优先消融AVNFP也可显著降低2V电压的左侧迷走神经干或右侧迷走神经干刺激下房颤的诱发率(分别降低了95.7％和96.3％),但联合消融SANFP+ AVNFP并不进一步显著降低左侧迷走神经干或右侧迷走神经干刺激下的房颤诱发率(分别较消融前降低了98.0％和100％).(3)优先消融SANFP或AVNFP均可显著抑制迷走神经干刺激引起的右房、左房及右上肺静脉部位的ERP缩短效应.与单独消融SANFP相比,联合消融SANFP+AVNFP可进一步抑制迷走神经干刺激引起右房ERP的缩短效应,而联合消融AVNFP+ SANFP对迷 走神经干刺激引起左、右心房及肺静脉ERP的缩短效应的抑制作用与单独消融AVNFP比较差异无统计学意义.结论 心外膜脂肪垫消融可改变迷走神经干刺激对房颤诱发及心房肌、肺静脉ERP的影响,其中AVNFP是迷走神经干支配心房的汇聚点和主控区,因此AVNFP可能是房颤神经消融更有效的靶点.     

犬急性心房颤动电重构现象的实验研究

目的 观察短阵心房颤动(房颤)的电重构现象及其恢复过程，探讨电重构与房颤再发及维持的关系。方法 15只健康成年犬于左、右心房外膜7个部位缝合双极记录电极，自心耳给予600次／min起搏诱发2h房颤，其中5只犬每间隔10min测量左、右心耳的心房有效不应期(AERP)，观察其恢复过程；另10只犬在房颤前后分别测量在起搏周长350ms、250ms、200ms时7个部位的AERP并记录电生理检查时房颤的诱发率及其持续时间。结果 2h房颤后心房各点AERP显著缩短，对心率适应不良，AERP离散度增高，继发性房颤诱发率增高、持续时间延长。AERP缩短可持续30min，60-80min后恢复。左心耳AERP恢复过程慢于右心耳。可诱发房颤的部位AERP更短，与继发性房颤的平均持续时间呈显著性负相关。可诱发房颤的心房其AERP离散度明显增高，但与继发性房颤的持续时间无关。AERP心率适应不良部位继发性房颤的诱发率高于生理性AERP心率适应性部位。低位右心房及左心耳部位的期前兴奋易于诱发房颤。结论 2h诱发的房颤足以使健康心房发生类似持续性房颤的电重构，电重构使房颤易于再发。AERP离散度与房颤的诱发有关，AERP缩短与房颤的持续性有关，房性早搏的发生部位与房颤的易患性有关。     

Renal sympathetic denervation suppresses postapneic blood pressure rises and atrial fibrillation in a model for sleep apnea

The aim of this study was to identify the relative impact of adrenergic and cholinergic activity on atrial fibrillation (AF) inducibility and blood pressure (BP) in a model for obstructive sleep apnea. Obstructive sleep apnea is associated with sympathovagal disbalance, AF, and postapneic BP rises. Renal denervation (RDN) reduces renal efferent and possibly also afferent sympathetic activity and BP in resistant hypertension. The effects of RDN compared with β-blockade by atenolol on atrial electrophysiological changes, AF inducibility, and BP during obstructive events and on shortening of atrial effective refractory period (AERP) induced by high-frequency stimulation of ganglionated plexi were investigated in 20 anesthetized pigs. Tracheal occlusion with applied negative tracheal pressure (NTP; at -80 mbar) induced pronounced AERP shortening and increased AF inducibility in all of the pigs. RDN but not atenolol reduced NTP-induced AF-inducibility (20% versus 100% at baseline; P=0.0001) and attenuated NTP-induced AERP shortening more than atenolol (27±5 versus 43±3 ms after atenolol; P=0.0272). Administration of atropine after RDN or atenolol completely inhibited NTP-induced AERP shortening. AERP shortening induced by high-frequency stimulation of ganglionated plexi was not influenced by RDN, suggesting that changes in sensitivity of ganglionated plexi do not play a role in the antiarrhythmic effect of RDN. Postapneic BP rise was inhibited by RDN and not modified by atenolol. We showed that vagally mediated NTP-induced AERP shortening is modulated by RDN or atenolol, which emphasizes the importance of autonomic disbalance in obstructive sleep apnea-associated AF. Renal denervation displays antiarrhythmic effects by reducing NTP-induced AERP shortening and inhibits postapneic BP rises associated with obstructive events.     

Inducibility of atrial fibrillation caused by acute increase of atrial pressure in rat diseased heart with chronic atrial dilation

Although acute atrial dilation facilitates the induction of atrial fibrillation (AF) in the normal heart, little is known about whether the induction of AF due to acute atrial dilation increases in the diseased heart. To clarify this, we compared the inducibility of AF by an acute increase of atrial pressure with and without chronic atrial dilation induced by volume- and pressure-overload in rats. Eight weeks after creating abdominal aortocaval shunt and aortic constriction rats (LVH rats, n = 8) or sham rats (n = 8), the hearts were perfused in Langendorff's manner. Right atrial (RA) pressure was increased from 2 cm H2O to 10 cm H2O by the height of the reservoir. Inducibility of AF was evaluated by 5 times burst pacing from the right atrium, and mean cycle length of AF (CL) and the atrial effective refractory period (AERP) were also measured. The inducibility of AF increased from 5 ± 3% at 2 cm H2O to 50 ± 5% at 10 cm H2O RA pressure in sham rats (P < 0.01), but not in LVH rats (20 ± 7% to 25 ± 6%, NS). Mean CL and AERP in LVH rats were longer than those in sham rats. In addition, the AERP decreased with an increase in RA pressure from 2 cm H2O to 10 cm H2O in sham rats, but not in LVH rats. The inducibility of AF caused by an acute increase of RA pressure did not increase in the diseased heart, suggesting that electrophysiological remodeling may play a role, at least in a compensated state, for the prevention of AF due to an acute increase of atrial pressure.