房室传导间期(A-V)的自动测量及频谱特征

目的 探讨房室传导间期(A-V)的自动测量,频谱特点及心率对其影响。方法 实验是在去神经的猫上进行,由右颈总动脉插入主动脉根部,测出希氏束(His)电图,通过模板匹配的方法自动检测His电图中心房(A)、希氏(H)波及心室(V)波,并将AA、AV间期数据通过快速傅立叶(FFT)转换,获得其频谱特征。再通过程序控制心房起搏观察了AA间期变化对AV频谱的影响。结果His束中A、H、V波可以自动重复检测,AV频谱与AA频谱均相似,但密度(PSD)较AA小,经标准化后,两者的高频(HF),低频(LF)及高频/低频(HF/LF)相同(P>0.05),通过心房起搏表明AA间期与AV间期呈非线形关系,AV频谱中HF与AA间期的变化率呈负相关(R=-0.97,P<0.01),LF与AA间期的变化率呈正相关关系(R=0.96,P<0.01)。结论心脏His束自动测量揭示了房室传导的频域特征以及心率对AV频谱各成份的相关关系,为研究心脏房室传导障碍性疾病以及心率对心电频谱的影响提供了一个新的方法。     

病窦综合征患者起搏器术后房室传导方式对Tei指数的影响

目的:评估固定的长AV间期下的DDD起搏模式对病态窦房结综合征(SSS)患者在减少心室起搏方面的效果;比较应用固定的长AV间期保留自身房室传导与最适AV间期下房室顺序起搏两种模式的优劣性,为此类患者选择具有最佳血流动力学效应的起搏参数设置提供临床依据。方法:连续选取2009年5月至2011年4月在我院因SSS而安置双腔心脏永久起搏器进行治疗的55位患者作为研究对象,分3次随访进行,每次随访时间间隔为2个月,将起搏器程控与超声测量相结合,进行两种不同AV间期下房室顺序起搏模式的血流动力学效应评估与对比。结果:与临床经验性AV间期相比,固定的长AV间期下的房室顺序起搏使心室起搏百分比由在31.8%降低至1.18%(P=0.00017);由最适AV间期下转为固定的长AV间期(350ms)下的房室顺序起搏模式后,心脏总体舒张和收缩功能指标(Tei指数)存在差异,且以左室Tei指数下降更为显著(0.67±0.17比0.45±0.09,P<0.0001)。结论:固定的长AV间期(350ms)下的房室顺序起搏能够有效减少心室起搏,且在血流动力学方面优于最适AV间期下的房室顺序起搏。     

双腔起搏器房室间期自动搜索功能对右心室起搏比例影响的临床研究

目的比较植入双腔起搏器患者房室（AV）间期自动搜索功能（Search AV）打开与固定长AV间期起搏,对右心室起搏比例的影响。方法入选60例病态窦房结综合征或间歇性Ⅱ度或Ⅲ度AV传导阻滞患者,均安装双腔起搏器。程控首先关闭Search AV功能,固定长AV间期（起搏房室间期220ms,感知房室间期200ms）起搏3个月,后程控打开Search AV 3个月,自身对照,比较其心房起搏比例、心室起搏比例及高频心房事件次数。再根据患者是否1：1房室传导分为2个亚组,自身对照分别比较其心房起搏比例、心室起搏比例及高频心房时间次数。结果58倒患者完成随访,固定长AV间期起搏时比Search AV（＋）自动搜索功能打开时的心室起搏比例、高频心房事件次数都高,分别为（70．5±12．4）％vs（22．4±8．3）％,（86±16）次VS（31±11）次（P=0．007,P=0．006）;而心房起搏比例二者差异无统计学意义。在1：1房室传导组（33例）及非1：1房室传导组（25例）两亚组比较中,均得出相同结果。结论Search AV功能可以减少不必要的右心室起搏,减少高频心房事件。     

有关食道心房调搏的几个问题

1.在做食道心房调搏时随着起搏频率的逐渐增加,起搏信号到QRS波群的时间刺激反应(S-R)有所延长,说明什么问题? 答:这是由于刺激脉冲落入前一个心搏所造成的房室传导组织(一般多在房室结处)的相对不应期中所致。起搏频率愈快,刺激脉冲落在相对不应期中的     

选择性刺激犬窦房结及房室结脂肪垫的实验研究

目的:心脏脂肪垫(CFP)含有支配窦房结(SAN)及房室结(AVN)的副交感神经纤维节.本文通过选择性刺激SAN及AVN CFP,观察其对SAN功能及房颤(AF)时房室传导的影响,以明确SAN及AVN CFP的神经功能分布特点.方法:取犬33只,经开胸直接刺激SAN及AVN CFP.刺激能量由0mA逐级增高直至AF诱发(频率20 Hz,脉宽0.2 ms).分别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直至最大值10.0 mA.记录诱发AF的连续10个RR间期,取其平均值.结果:75.8%犬SAN CFP刺激延长SCL>50%,无一只犬AVN CFP刺激延长SCL>10%.100%犬在SAN和AVN CFP刺激下诱发AF,阈值分别为(4.0±1.3)mA及(4.5±1.5)mA.直接SAN及AVN CFP刺激均延长AF的RR间期.结论:直接SAN及AVN CFP刺激均增加AF诱发的易感性,并延长AF时的房室传导时间.同时SAN CFP刺激还具有调节SAN的功能.     

心电图P波宽度在优化双腔起搏器房室间期中的价值

目的:探索以心电图P波宽度优化双腔起搏器房室间期(AV间期)的方法,以期获得良好的血流动力学效果。方法:选择63例因Ⅲ度或高度房室传导阻滞植入Medtronic双腔起搏器的患者,测量其心电图自身P波宽度,或从心房起搏脉冲至起搏P波末端的宽度,在此测量值上加100ms,设定为双腔起搏器的感知AV间期(SAV)和起搏AV间期(PAV)。每例患者分别在出厂常规设置的AV间期和根据心电图优化的AV间期设定值下进行超声心动图检查,比较即刻血流动力学参数。结果:经心电图优化AV间期后,患者左室舒张末容积(LVEDV)、左室收缩末期容积(LVESV)和左室射血分数(LVEF)均较常规出厂设置的AV间期有显著改善(69.5±11.2比72.3±12.7;29.5±9.5比27.88±10.07;63.6±5.3比67.2±6.2,P<0.05)。结论:根据心电图P波宽度优化双腔起搏器AV间期,可获得良好的血流动力学效果,左室充盈改善,LVEF上升;且该法简单易行,具广泛的临床实用价值。     

房室折返性心动过速伴RR间期长短交替发生机制的研究

目的探讨房室折返性心动过速(atrioventricular reciprocating tachycardia,AVRT)伴RR间期长短交替的发生机制。方法回顾性分析2009年8月至2016年8月,在泰达国际心血管病医院心内科经导管射频消融治疗的AVRT患者317例临床资料,AVRT时给予异博定5 mg,缓慢静脉推注10 min,给药后观察是否有RR间期、AH间期、HV间期和VA间期变化,以及变化发生的时间。结果给予异博定后有8例患者发生RR间期长短交替,并且均伴QRS波电交替,RR间期长短交替现象发生时均为相邻心搏的AH间期差值逐渐延长,无AH跳跃,HV间期和VA间期恒定,此现象发生于给药后6~17 min,心动过速平均周期比给药前延长16~42 ms;3例患者RR间期长短交替现象消失时均为相邻心搏的AH间期差值逐渐缩短,无AH跳跃,HV和VA间期恒定,直至AH间期相等,消失时间为给药后19~57 min;5例患者给药后AVRT终止。结论由此推断其发生机制是由于心动过速时AH间期频率依赖性递减传导所致,这一心电现象不能被程序刺激诱发。     

经皮冠状动脉介入治疗急性下壁心肌梗死的临床分析

目的 分析经皮冠状动脉介入治疗(PCI)急性下壁心肌梗死(AIMI)的特点,以提高诊治水平.方法 选择冠状动脉造影确诊的AIMI患者151例,其中男性145例,女性6例.回顾性分析梗死相关动脉的特点及PCI术前、术中无复流发生率等临床特点.结果 与<12 h组比较,12 h后行PCI无复流率(53.8%vs 15.8%,P<0.01)和低血压发生率(80.8%vs 36.8%,P<0.01)明显增加,再灌注心律失常发生率两组比较差异无统计学意义;与正常窦律组比较,房室传导阻滞(AVB)组右冠状动脉优势型居多(84.4%vs 63.0%,P<0.01),无复流率增加(53.1%vs 13.9%,P<0.01);使用Diver CE明显降低无复流的发生(24.3%vs 9.1%,P<0.01).结论 尽早行PCI是抢救AIMI患者的关键措施.伴有AVB或低血压时,即使时间超过24 h亦应进行PCI.使用血栓抽吸导管可有效降低无复流的发生.经使用过的球囊注入尿激酶治疗无复流,是简单实用、经济、有效的方法.     

病态窦房结综合征伴房室传导延迟患者心房按需起搏与房室同步起搏模式左心功能的超声评价

目的 运用多普勒超声心动图及组织多普勒(TDI)技术评价病态窦房结综合征(SSS)伴房室传导延迟患者分别在心房按需起搏(AAI)与房室同步起搏(DDD)模式下的心脏功能,并探讨其起搏模式的选择.方法 选择植入DDD起搏器的SSS伴Ⅰ度房室传导阻滞的患者24例,分别置于AAI模式和房室间期优化的DDD模式,应用多普勒超声心动图和TDI技术评价这两种起搏模式下心脏的收缩和舒张功能.结果 多普勒超声心动图评价心脏收缩功能(EF,主动脉VTI)和舒张功能(E/A)参数在AAI组和DDD组之间差异无统计学意义.TDI显示收缩峰值速度(Sm)在AAI组为(10.88±2.92)cm/s,DDD组为(9.06±2.49)cm/s;舒张早期峰值速度(Em)、舒张早期峰值速度/舒张晚期峰值速度(Em/Am)在AAI组和DDD组分别为[(9.25±2.89)cm/s 对 (8.37±2.31)cm/s、0.96±0.35 对 0.80±0.25];Tei指数在AAI组为 0.56±0.12,DDD组为 0.80±0.40.这些参数在两组间差异有统计学意义(P《0.05).结论 ①SSS伴房室传导延迟(PR》200 ms且《260 ms)患者采用AAI起搏模式心脏收缩和舒张功能的改善优于DDD起搏模式;②TDI技术较多普勒超声心动图能更敏感地反映心脏收缩和舒张功能的变化.     

右心室心尖部与流出道间隔部起搏对QRS波时限、QT间期及Tp-e间期的影响

目的观察右心室心尖部(RVA)与右心室流出道间隔部(RVOT)起搏对患者体表心电图QRS时限、QT间期及Tp-e间期的影响。方法选取因阵发性室上性心动过速在南京市鼓楼医院行射频消融的患者18例,术中将心室电极分别放置于右心室流出道间隔部及右心室心尖部,给予S1S2刺激,并测量S2刺激后体表心电图的QRS间期、QT间期和Tp-e间期。结果电生理检查结果显示:同RVA起搏比较,RVOT起搏后QRS时限明显缩短[(131.31±10.00)msvs.(156.40±13.16)ms,P<0.001],QT间期[(334.62±11.75)msvs.(351.09±20.13)ms,P<0.01]及Tp-e间期[(71.97±13.03)msvs.(83.48±14.81)ms,P<0.05)]也明显缩短,其差异均具有统计学意义。结论同心尖部起搏比较,右心室流出道间隔部起搏对QRS波时限、QT间期及Tp-e间期有明显的影响。     

Nonuniformity of AH Intervals During Stimulation at Different Left Atrial Sites

Studies in humans have found left atrial stimulation via the coronary sinus (CS) to elicit significantly shorter atrium-His (AH) intervals as compared to right atrial stimulation, but whether pacing at dijferent left atrial sites (anterior vs posterior left atrium, i.e., far distal vs proximal CSJ affects the AH interval has not been studied. Hence, in 22 patients, we compared the effects of stimulation from various atriai sites, including anterior high right atrium (HRA), distal CS, mid-CS, and proximal CS, on; stimulus-atrium (SA), AH, and stimuIus-His intervals on the His bundle electrogram. Paced cycle length differed for each patient (range 900–350 msec, mean 532 ± 140 msec), but conduction intervals from different atrial sites were compared using identical cycle length in each patient. The mean SA intervals were 34 ± 10 msec, 57 ± 10 msec, 44 ± 11 msec, and 32 ± 8 msec with stimulation, respectively, from HRA, distal CS, mid-CS. and proximal CS (each significantly different except for HRA vs proximal CSJ. The mean AH intervals were 123 ± 23 msec, 104 ± 28 msec, 95 ± 15 msec, and 90 ± 18 msec with stimulation, respectively, from HRA, distal CS, mid-CS, and proximal CS (each significantly different except for mid-CS vs proximal CSJ. In 13 patients, the discrepancy in AH intervals during distal versus proximal CS stimulation was > 15 msec; in 9 patients this difference was only < 10 msec, considered within the range of measurement error. Thus, in a significant portion of patients, discrepant AH intervals were demonstrated during stimulation from the distal versus proximal CS. These previously undescribed observations suggest that electrophysiological studies on atrioventricular nodal conduction that involve left atrial stimulation must take into account actual location of the stimulation site (anterior or posterior) in order to properly interpret the findings.     

Effects of Increasing Heart Rate Induced by Efferent Sympathetic Neuronal Stimulation, Isoproterenol or Cardiac Pacing on Myocardial Function and Oxygen Utilization

The effects of increasing heart rate by six different methods on cardiac /unction were investigated in 17 open-chest anesthetized dogs. Heart rate was increased approximately 30% by (1) right interganglionic nerve stimulation, (2) atrial pacing, (3) ventricular pacing, (4) atriovenfricular sequential pacing, (5) right stellate ganglion stimulntion, and (6) isoproterenoi administration. During heart rate increases induced by atrial pacing left ventricular intramyocardial pressure, coronary Wood flow, oxygen delivery per unit of myocardial oxygen consumption, and myocardial efficiency were unchanged. Ventricular pacing reduced left ventricular cavity and septal intramyocardial pressure, while circumflex coronary flow increased, resulting in reduced oxygen delivery relative to myocardial oxygen consumption. Similarly, atrioventricu-lar sequential pacing increased circumflex coronary artery flow and myocardial oxygen consumption, and decreased septal intramyocardial pressure and oxygen delivery per unit of myocardial oxygen consumption. Right stellate ganglion stimulation and isoproterenol increased left anterior descending and circumflex coronary artery blood flow, intramyocardial pressure, and myocardial oxygen consumption. Estimated myocardial efficiency (left ventricle) was decreased by ventricular pacing and isoproterenol, and was unchanged by atrial pacing and right interganglionic nerve stimulation. Increases in heart rate induced by right interganglionic nerve stimulation did not alter myocardial oxygen consumption, or the index of cardiac efficiency. It is concluded that augmentation of heart rate by either ventricular or atrioventricular pacing impairs myocardial function so that there is a decrease of left ventricular efficiency, and isoproterenol augments chronotropism and myocardial force relative to cardiac external work so there is a reduction in cardiac efficiency. In contrast, atrial pacing or right interganglionic nerve stimulation augments chronotropism such that myocardial oxygen consumption and efficiency are unchanged.     

心肌缺血对心电频谱的影响

目的研究缺血对心电频谱的直接影响。方法在去自主传出神经的动物上,通过结扎右冠状动脉造成心肌缺血的动物模型,测量两心房间期(AA)和心房波与心室波间期(AV),采用快速傅立叶转换(FFT)的方法将期转换为频域函数进行分析。结果缺血后,AA间期频谱低频由(8.2±3.2)nu升高为(23.6±18.9)nu(P<0.01),高频由(80.0±7.1)降低为(59.4±23.9)nu(P<0.01);AV频谱低频由(16.4±10.5)nu升高为(31.4±11.3)nu(P<0.01),高频由(72.1±11.6)nu降低为(54.4±13.4)nu(P<0.01)。结论在去自主神经状态下,结扎右冠状动脉后AA、AV频谱均出现低频升高,高频显著下降。因此缺血是心电频谱改变的一个独立的直接因素。     

The Importance of the Left Atrioventricular Interval during Atrioventricular Sequential Pacing

During atrioventricular (AV) sequential pacing from the right heart, the interval between the left atrium and ventricle may vary from the programmed AV interval depending on the position of the atrial and ventricular electrodes and interatrial and interventricular conduction. The aim of this study was to determine the hemodynamic effects of altering the left AV interval while keeping the programmed AV interval constant. Four male and 17 female patients, aged 49 ± 15 years were studied. The left AV interval was measured by a catheter in the coronary sinus. Stroke volume and mitral flow were measured by simultaneous echo Doppler during AV sequential pacing from the right atrial appendage and right ventricular apex at programmed AV intervals of 100. 60, and 6 ms. The atrial catheter was then positioned on the atrial septum and the measurements repeated. With the atrial catheter in the right atrial appendage, interatrial activation time (118 ± 20 ms) was similar to interventricular activation time (125 ± 21 ms) and the left AV interval was almost identical to the programmed right AV interval. There was a significant correlation between interatrial and interventricular activation times (r = 0.8; P < 0.001). Positioning the atrial electrode on the septum decreased interatrial activation time by 39 ± 12 ms and increased the left AV interval by a similar amount. At a programmed AV interval of 60 ms, the left AV interval increased from 67 ± 15 ms to 105 ± 17 ms after the atrial catheter was repositioned from the appendage to the septum (P < 0.001). Compared to pacing from the right atrial appendage, atrial septal pacing increased mitral A wave velocity integral (2.8 ± 1.4 vs 4.4 ±1.7 cm at a programmed AV interval of 60 ms, P < 0.01), decreased E wave velocity integral (8.1 ± 2.2 vs 6.1 ± 2.4 cm, P < 0.001) but did not alter stroke volume (44.8 ± 10.6 vs 44.9 ± 10.1 mL). In contrast, a 40 ms decrease in the programmed right AV interval from 100 to 60 ms decreased stroke volume from 48.0 ± 10.0 to 44.9 ± 10.2 mL (P < 0.001). There was a strong relationship between interatrial and interventricular conduction so that patients with prolonged interatrial conduction still had equivalent left and right AV intervals during atrioventricular sequential pacing from the right atrial appendage and right ventricular apex. Positioning the atrial electrode on the septum decreases interatrial activation time and increases the left AV interval by about 40 ms but has minimal hemodynamic effect in patients without heart failure.     

迷走神经对心房电生理特性的调节在犬心房电重构中的变化

目的研究迷走神经对心房电生理特性的调节在心房电重构中的变化。方法成年杂种犬9只,麻醉后分离双侧颈部交感-迷走神经干。给予美托洛尔阻断交感神经的影响。在右心房（RA）、冠状静脉窦（CS）和右心室（RV）放置多极导管。消融希氏束完全阻断房室结并植入右室临时起搏器。通过RA导管进行600次／min的起搏30min构建急性心房电重构模型。在心房电重构前后测量基础状态（无迷走神经刺激）和迷走神经刺激下的心房有效不应期（ERP）和房颤易感窗口（VW）。结果在基础状态下,ERP在心房电重构后明显缩短（P〈0.05）。迷走神经刺激下,ERP在心房电重构后也明显缩短（P〈0.05）。基础状态下,在心房电重构前后均不能诱发房颤（VW接近0）。迷走神经刺激时,房颤易感窗口在心房电重构后明显增大（P〈0.05）。结论短期的心房电重构能够缩短心房的有效不应期。心房电重构伴随着迷走神经对心房电生理特性的调节发生改变,导致迷走神经介导性房颤的易感性增加。     

Altered intracardiac conduction after acute administration of ethanol in the dog.

Varying concentrations of ethyl alcohol were injected either into the left main coronary artery or intravenously in anesthetized intact dogs. Effects of alcohol on intracardiac conduction (by His bundle electrogram) were examined at spontaneous and paced (atrial) heart rates. Alcohol by the intracoronary route prolonged atrioventricular node and intraventricular conduction times by approximately 5 to 15%. These changes preceded a depression of left ventricular systolic pressure and of the rate of rise of left ventricular pressure and an elevation of left ventricular end-diastolic pressure. Intracoronary injections of contrast medium (sodium diatriozoate) or iso-osmolar solutions of sucrose and injections of similar amounts of alcohol in the ascending or descending aorta did not affect intracardiac conduction. Increasing atrial pacing rates resulted in prolongation of atrioventricular nodal conduction intervals, but did not influence intraventricular conduction time. At each pacing rate, alcohol depressed both atrioventricular nodal and intraventricular conduction. The data suggest that alcohol has a direct depressant effect on intracardiac conduction.     

Evaluation of acute stress-induced regional myocardial ischemia: Comparison of regional contractile and metabolic indices to easily accessible global left ventricular indices

In clinical studies stress-induced myocardial ischemia in patients with coronary artery disease is used to evaluate the severity of this disease. The discussion on the importance of some parameters measured during this intervention is controversial, other parameters are difficult to obtain. On the basis of an experimental model of stress-induced myocardial ischemia, we tried to find an index that reflects best this cardiac state. We therefore compared in eight anesthetized open-chest dogs control conditions with three other hemodynamic states with increasing imbalance between myocardial oxygen demand and oxygen supply: severe stenosis on circumflex coronary artery, 60 s cardiac sympathetic nerve stimulation (CSNS) with a severe stenosis on circumflex coronary artery, and 60 s complete occlusion of circumflex coronary artery. Using a one-way analysis of variance, we found two significantly changed parameters during the stress-induced ischemia: Regional lactate extraction was turned to production (32 +/- 4 vs. -4 +/- 1%) and the ratio of dP/dtmin to dP/dtmax was decreased (1.13 +/- 0.05 vs. 0.67 +/- 0.05; control vs. CSNS with a severe stenosis on circumflex coronary artery). We conclude that the ratio of dP/dtmin to dP/dtmax is an easily accessible, sensitive, and dynamic index for characterization of an stress-induced myocardial ischemia.     

Soluble L-selectin and neutrophil derived oxidative stress after pacing induced myocardial ischemia in chronic stable coronary artery disease

We studied the effect of atrial pacing induced myocardial ischemia on levels of soluble L-selectin (sL-selectin) and generation of neutrophil derived reactive oxygen species (ROS) in 10 patients with coronary artery disease (CAD) and stable angina and in six individuals without CAD. Myocardial ischemia was measured metabolically by lactate sampling from the coronary sinus (CS) and arterial blood at each pacing step. Before each pacing step, at peak pacing and shortly after cessation, plasma concentrations of sL-selectin and generation of ROS using the chemiluminescence method were measured in CS and femoral artery blood. Baseline sL-selectin levels in CS samples were significantly lower in the CAD compared to the control group (547 +/- 80 vs 836 +/- 82 ng/mL, P = 0.03). At peak pacing, nine of ten patients with CAD developed myocardial ischemia (lactate extraction ratio at rest 28% +/- 7%, at peak pacing -16% +/- 6%). In these patients, luminol-enhanced chemiluminescence (CL, 0.88 +/- 0.45 vs 1.9 +/- 0.9 cpm x 10(5), P = 0.09) and levels of sL-selectin (547 +/- 80 vs 764 +/- 86 ng/mL, P = 0.03) from naive neutrophils increased significantly in CS blood suggesting a potent in vivo activation of neutrophils. In control patients, incremental pacing caused neither myocardial ischemia nor a significant change of chemiluminescence or of sL-selectin levels. In conclusion, myocardial ischemia induced by pacing tachycardia is able to activate neutrophils in patients with chronic stable coronary artery disease leading to increased generation of ROS and shedding of L-selectin into the coronary circulation.     

Cardiac electrophysiologic and hemodynamic activity of pimobendan (UD-CG 115 BS), a new inotropic agent

The hemodynamic and cardiac electrophysiologic properties of pimobendan, a new pyridazinone-benzimidazole type inotropic agent, were studied in urethane-anesthetized dogs. The cumulative i.v. administration of 0.1, 0.3, and 1.0 mg/kg pimobendan caused a dose-dependent decrease in mean arterial pressure and an increase in sinus heart rate. When heart rate was maintained constant by overdrive atrial pacing, hemodynamic changes in response to pimobendan consisted of dose-related increases in right ventricular isometric contractile force (P less than .05 at 0.3 and 1.0 mg/kg), left ventricular +dP/dt (P less than .05 at 0.3 and 1.0 mg/kg), and left circumflex coronary artery blood flow (P less than .05 at 1.0 mg/kg). Increases in each of the aforementioned hemodynamic parameters were sustained for up to 4 hr after the i.v. administration of 1.0 mg/kg pimobendan. The cardiac electrophysiologic changes associated with pimobendan administration included decreases in the atrial (P less than .05 at 1.0 mg/kg), ventricular (P less than .05 at 0.3 and 1.0 mg/kg), and atrioventricular nodal functional (P less than .05 at 0.3 and 1.0 mg/kg) and effective (P less than .05 at 1.0 mg/kg) refractory periods. Atrioventricular conduction velocity was enhanced after pimobendan, as indicated by a shortening of the AH (P less than .05 at 0.3 mg/kg and at 1.0 mg/kg) and PR intervals (P less than 0.05 at 1.0 mg/kg). Pretreatment with propranolol (0.5 mg/kg i.v.) attenuated the pimobendan-induced decrease in the ventricular refractory period and the increase in heart rate, whereas the decrease in arterial pressure was enhanced. These results indicate that the i.v. administration of pimobendan to anesthetized dogs produces a dose-related positive inotropic effect, coronary and peripheral vasodilation, and cardiac electrophysiologic effects that include decreases in atrial, atrioventricular, and ventricular refractoriness as well as a facilitation of atrioventricular conduction. The observed electrophysiologic changes may be mediated, in part, by a baroreceptor-mediated increase in sympathetic nervous system activity.     

超速起搏预处理对急性心肌梗死的延迟保护

目的　探讨超速心室起搏 (ventricularoverdrivepacing,VOP)预处理对急性心肌梗死的延迟保护作用 (delayedprotection ,DP)及可能机制。方法　 2 0只兔随机分为 4组 :(1)对照组 ,将电极导管送至右心室旷置 70min ,2 4h后结扎、冠状动脉左前降支造成缺血再灌注模型。 (2 )起搏组 ,缺血再灌注前 2 4h予VOP。 (3)放线菌素组 ,缺血再灌注前 2 4h静注放线菌素D阻滞热休克蛋白 (HSP)转录。 (4 )起搏 放线菌素组 ,延迟缺血再灌注前 2 4h予VOP并静脉注射放线菌素D ,缺血再灌注前后测定血流动力学变化 ,以TTC染色测量各组心肌梗死面积百分比 ,免疫组化染色间检测HSP70抗原 ,并观察心肌缺血再灌注后的组织学改变。结果　与对照组比较 ,起搏组心肌梗死面积减少 34 35 % (P <0 0 0 1) ,左心收缩和舒张功能均改善 ;心肌超微结构损伤减轻。其余组与对照组比较 ,在各项指标上差别无显著意义。HSP70免疫组化染色仅在起搏组心肌标本呈阳性。结论　多次VOP预处理对急性梗死心肌有明显的延迟保护作用 ,此作用与HSP70的表达密切相关。