参附注射液在短时间内对窦房结功能的影响

目的探讨参附注射液在短时间内（30min）对窦房结功能的影响：方法选择窦房结功能正常病例6例和病态窦房结综合征（SSS）病例10例，采用食道电生理的方法观察参附注射液静脉注射前后窦房性恢复时间（SNRT）、校正窦房结恢复时间（CSNRT）、窦房结传导时间（SACT）、心率（HR）的变化。结果窦房结功能正常病例和SSS病例，在参附注射液静脉注射前后SNRT、CSNRT、SACT、HR均无统计学意义（P〉0．05）。结论参附注射液对窦房结功能正常和SSS病人的窦房结功能在短时间内无影响。     

食道电生理检查在窦性心动过缓中的应用

目的探讨食道电生理检查在窦性心动过缓(SB)中的临床应用价值。方法回顾分析纳入342例经体检及门诊诊断为SB的患者,依据心率50bpm(68例,占19.8%)及≥50bpm(274例,占80.0%)而分为二组,并按性别、不同年龄段、有无症状分组,所有患者均行十二导心电图(ECG)、动态心电图检查(DCG)、药物前后食道电生理检查。结果 342例患者中检出窦房结功能障碍者58例,占16.9%,275例为迷走神经张力过高导致的窦性心动过缓,占80%,窦房结伴房室结功能低下者9例,占0.02%。心率50bpm及≥50bpm在窦房传导时间(SACT)无差异,而在窦房结恢复时间(SNRT)、校正窦房结恢复时间(CSNRT)有统计学差异(p0.05),心率50bpm组迷走神经张力明显高于无症状组。随年龄增长,SACT、SNRT、CSNRT值越大,迷走神经张力渐低,差异有统计学意义。有症状组其SNRT、CSNRT明显延长,差异有统计学意义。结论SB中年龄越大,窦房结功能障碍的发生率越高,年龄越轻,则迷走神经张力增高仍然是SB的主要原因。单纯SB的程度对于诊断窦房结功能障碍无明显临床价值,需结合患者年龄,通过食道电生理检查评价,此检查安全、无创、操作简便,具有独特而重要的临床价值,适宜临床推广应用。     

心内测定老年人窦房结恢复时间和窦房传导时间的报告

目的:探讨心内测定老年人窦房结恢复时间(SNRT)、校正的窦房结恢复时间(CSNRT)和窦房传导时间(SACT)的正常值。方法:对53例无病态窦房结综合征的老年人进行经皮右心房电生理检查,测定其SNRT和SACT。结果:53例老年人SACT98.7±34.4ms(51～222ms);SNRT1058.5±275.7ms(602～2260ms);CSNRT266.1±177.6ms(79～1189ms)。发现SNRT>1500ms,CSNRT>600ms各1例,SACT>150ms者有3例。结论:老年人心内测定的SNRT、CSNRT与文献中食道调搏法测定的无显著差异,而SACT则明显低于食道调搏法(P<0.01),与刺激部位有关。     

静注腺苷作为诊断病窦综合征的一种无创性试验

以往在病窦综合征(SSS)诊断中,窦房结恢复时间(SNRT)及校正的窦房结恢复时间(CSNRT)都需通过侵入性电生理检查测定。该文通过静注腺苷测定SNRT与CSNRT,并将其与侵入性电生理测定的结果相比较,从而说明静注腺苷测定SNRT与CSNRT作为一种无创性检测手段,在SSS诊断中的意义。     

心房程序刺激法（S1S2法）判断窦房传导时间的临床应用（摘要）

窦房传导时间(SACT)和窦房结恢复时间(SNRT)是目前临床心脏电生理检查中判断窦房结功能的两种主要指标。但由于SACT测定方法本身的局限性,其判断窦房结功能时的意义远不如SNRT大。因此,近来有作者提出以心房程序早搏刺激法(S_1S_2法)来测定SACT。本文通过非侵入性电生理测定方法初步探讨了其临床应用价值。     

快速起搏肺静脉对窦房结功能的影响及自主神经在其中的作用

探讨快速起搏肺静脉对窦房结功能的影响及自主神经在其中的作用。22条犬随机分为对照组、阿托品组、美托洛尔组和阿托品+美托洛尔组(简称阿+美组),测量药物注射前后以及经肺静脉以最大1∶1频率快速起搏心房 10min后的窦房结恢复时间(SNRT)和校正SNRT(CSNRT)。结果:①阿托品缩短SNRT和CSNRT,美托洛尔则延长SNRT和CSNRT,二者同时注射表现为SNRT和CSNRT缩短;②快速起搏 10min前后相比, 4组SNRT和CS NRT均延长。③与对照组相比,阿托品组和阿+美组显著减小SNRT延长的程度;与对照组相比,阿托品组显著减小CSNRT延长的程度,美托洛尔组显著增加CSNRT延长的程度。④与基础状态相比,对照组和美托洛尔组SNRT和CSNRT均显著延长。结论:短时间的快速起搏能够影响窦房结功能,引起窦房结电重构。阻断迷走神经能够阻止窦房结的电重构,单独阻断交感神经则无此作用。     

动态心电图心率趋势分析对SSS者起搏器安装的参考价值

动态心电图(DCG)监护是评价窦房结功能(SAF)的检测方法之一,因其方便、无痛苦,易于被患者接受,近年来普遍应用。对病态窦房结综合征(SSS)患者安装起搏器适应症,目前多依靠经食管心房调搏或心内电生理检测法测定其窦房结恢复时间(SANRT)、窦房传导时间(SACT)和固有心率(IHR)等了解和评估窦房结功能的好坏以及体内起搏器     

美托洛尔测定心脏固有心率的临床观察

目的　探讨 β1 受体阻滞剂——美托洛尔替代普奈洛尔测定心脏固有心率 (IHR)的可行性。方法　 6 0例受检者根据静息状态下的基础窦性心率分为 2组 :窦性心动过缓组 (心率低于 6 0次 / min,n=35 ) ;窦房结功能正常组(心率≥ 6 0次 / min,n=2 5 )。两组病人均以美托洛尔 5 mg与阿托品 2 mg混合一次性静脉注射测定 IHR,同时应用经食管心房调搏方法测定阻断自主神经前后的窦房结恢复时间 (SNRT)和校正窦房结恢复时间 (SNRTc)。结果　正常组的 IHR为 90 .2± 8.7次 / min;在窦缓组中 ,2 1例 SNRT和 SNRTc异常者 (窦缓 A组 )的 IHR为 6 7.1± 7.9次/ m in,14例 SNRT和 SNRTc正常者 (窦缓 B组 )的 IHR为 84.2± 16 .2次 / m in,A、B两亚组之间的 IHR值有显著性差异 (P<0 .0 1)。结论　美托洛尔与阿托品混合静脉注射能够理想地阻断自主神经系统对窦房结的影响 ,真实显示窦房结固有的自律性功能。     

病态窦房结综合征心房按需起搏后双结功能的转归探讨

为了解心房按需起搏术后窦房结和房室传导功能的远期转归,观察22例植入AAI起搏器患者术后30～102个月的双结功能电生理参数,并与术前比较.结果显示:术后SACT、SNRT、CSNRT、房室传导文氏阻滞点、2:1阻滞点与术前比较差异均无显著意义(P>0.05).认为AAI起搏器植入对病态窦房结综合征患者窦房结功能和房室传功能没有显著影响,也无起搏器依赖性.     

静注腺苷对病态窦房结综合征的诊断价值

病态窦房结综合征(SSS)病人需植入新的起搏器的比例上升到20％至50％,通常需用侵入性的电生理检查测定窦房结恢复时间(SNRT)和校正的窦房结恢复时间(CSNRT)来确定诊断。但由于电生理学检查花费大和为侵入性的操作,临床应用受到限制。腺苷是一广泛存在的天然代谢物质,对心率、心脏收缩力、平滑肌张力、释放神经介质,对糖、脂肪分解和肾、血小板、白细胞及内皮细胞功能有作用,并有镇静     

Functional and morphological organization of the guinea-pig sinoatrial node compared with the rabbit sinoatrial node

The primary pacemaker, i.e. the group of pacemaker cells discharging the sinoatrial node comprises less than 1000 cells in the guinea-pig and about 5000 cells in the rabbit. These primary pacemaker cells are described as 'central nodal' cells in light microscopy and as 'typical nodal' cells in electron microscopy. The action potential of the leading cells has a higher upstroke velocity in the guinea-pig than in the rabbit (6.2 v. 1.9 V/s). Gap junctions have been observed even in the very center of the node in both species. A zone of double-component action potentials at the septal margin of the node was observed in the rabbit, but not in the guinea-pig. Evidence is presented for abrupt transitions in electrophysiological as well as in ultrastructural characteristics in the guinea-pig sinoatrial node. The differences in intrinsic cycle length between both species but also between individuals of the same species are discussed.     

The mammalian sinoatrial node

Summary The sinoatrial node (SAN) was discovered in 1906 by Keith and Flack. The relation between its ultrastructure and function was first studied by Trautwein and Uchizono in 1963, whereas this relation was definitely established by Taylor and coworkers in 1978.The impulse originates from cells with a relatively low percentage of myofilaments. Earliest discharge is restricted to one site only in rabbit, guinea pig, cat, and pig and presumably also in larger animals. From this primary pacemaker area, the impulse is preferentially conducted towards the crista terminalis. The amount of cells in the primary pacemaker area may vary from a few hundred to a few thousand. In rabbit, guinea pig, cat, and pig, the amount of collagen is considerable. Normal SAN function was observed in the cat although the SAN volume occupied by myocytes was less than 5%. Changes in ionic composition of the perfusion fluid and the addition of autonomic substances may cause pacemaker shifts and altered activation patterns.     

Functional morphology of the pig sinoatrial node

The porcine sinoatrial node in an isolated right atrium preparation is characterized by unifocal impulse generation. It has a rather elongated shape and the larger part of its volume is taken up by collagen and fibroblasts. The impulse appears to emerge from a site where the percentage of myofilaments is relatively low. The impulse is propagated faster towards the crista terminalis than to the interatrial septum with preference for the oblique-upward direction. A very large zone of cells with low excitability is located at the interatrial septal side of the node.     

Modulated parasystole originating in the sinoatrial node

A computer model of "modulated sinus parasystole" was devised in which two sinus pacemakers interacted electrotonically, entraining each other's periodicity according to their beat-to-beat phasic relationships. Depending on the preestablished rules, the model gave rise to various rhythm patterns that were similar to those recorded in patients with sinoatrial arrhythmias. The validity of the model in predicting clinically observed rhythm disturbances was tested in a case of sinoatrial extrasystolic activity. The sinoatrial origin of parasystolic discharges giving rise to various patterns of group beating in this case was diagnosed according to the following electrocardiographic criteria: premature P waves having contour identical to P waves of basic beats, variable coupling intervals, and absence of compensatory pauses (i.e., returning cycles having duration similar to that of the basic P-P interval). For the analysis, it was assumed that two distinct but closely apposed sinoatrial pacemaker centers were competing for activation of the heart. The model accurately simulated the arrhythmias in the electrocardiographic trace. The best fit was found when the two pacemakers interacted on the basis of "resetting" in one direction and electronic modulation in the other. In fact, under appropriate conditions, the model matched precisely all frequency-dependent patterns of extrasystolic activity observed in the trace. We conclude that the modulated parasystole hypothesis can readily explain the mechanism of sinus extrasystolic discharges whose returning cycle equals the basic P-P interval. Moreover, the model predicts that, when the rules for mutual entrainment between "dominant" and parasystolic sinus pacemaker are appropriate, the returning cycle can be shorter than the basic cycle.     

Light microscopy of sinoatrial node ischaemia

Ischaemia of the sinoatrial node (SAN) region was produced in 57 dogs by obstructing the sinoatrial nodal artery by injecting it with various media. In the light microscope ischaemia of the nodal cells resulted in myocytolysis. The cells were oedematous, with a distinctly cleared cytoplasm and cytoplasmic vacuolization. Macrophages penetrated into the nodal cells. Myocytolysis resulted either in disintegration of the cell membrane and the nucleus or in atrophy of nodal cells. The damaged cells were gradually replaced with collagenous connective tissue. Ischaemic changes in the light microscope appeared between hours 3 to 24 after the onset of ischaemia and continued to develop for a period of 4 to 5 weeks showing a variable intensity in different areas of the SAN region. The process became virtually stabilized between months 1 to 7. The degree of ischaemia was most probably responsible for the fact that changes of various degree--myocytolysis, atrophy and fibrosis--were present simultaneously. The preservation of ganglion cells in ischaemic tissue is discussed.     

Physiopathology of the sinus node and sinoatrial conduction

New information about the pathophysiology of the sinus node and sino-atrial conduction has been published in the last few years. The sinus node consists of cells separated by a network of collagen fibres. This anatomical disparity explains the different electrophysiological characteristics of the node; the morphology of cellular action potentials depends on the site of recording. The dominant and most automatic pacemaker cells are situated in the cephalic region and the latent pacemaker cells in the caudal region. However, synchronisation of these different cellular activities is possible and results in a coherent signal. This complex synchronisation has been the object of several recent papers. The phenomenon of intrasinusal pacemaker shift and the stimuli which induce it have been studied in depth. In general, positive chronotropic stimuli tend to shift the dominant pacemaker towards the cephalic part and negative chronotropic stimuli towards the caudal part of the node. It is possible to assess pacemaker shift clinically and this phenomenon must be taken into consideration when studying sinus node function. Intercellular conduction and especially electrotonic conduction does not play a role in the genesis of the flux, which represents spontaneous cellular automatism, but in its mode of expression, that is to say the sinus rhythm. The pathophysiology of sinoatrial block is complex because it may be situated within and/or around the sinus node. The extrinsic or intrinsic mechanisms of these blocks may be interrelated. Variations in sinus rhythm must be taken into account in the genesis of sinoatrial block; an acceleration in rhythm may block conduction in the perisinusal region. Finally, our knowledge of the ionic fluxes underlying sinus automatism has also improved with individualization of the pacemaker current (if).(ABSTRACT TRUNCATED AT 250 WORDS)