Anatomical variants of sinoatrial and atrioventricular node arteries

The authors investigated on 70 hearts taken from deceased subjects of either sex, aged 19 to 75 years, anatomical variants of sinoatrial (SAN) and atrioventricular node (AVN) arteries. As regards the branching of the SAN artery from the right and left coronary artery (RCA, LCA), they found altogether 14 variants of connection with the anterior atrial sulcus and the orifice of the superior vena cava. As regards the branching of the AVN from the RCA and the LCA, they identified altogether 6 variants of connection with the venous sinus orifice and the base of the interventricular septum. Problems of surgical interventions on SAN and AVN arteries and mechanisms of possible traumatization in the course of these operations are discussed. Surgical lesions can be prevented by thorough analysis of coronarograms and by taking into account anatomical variants of SAN and AVN arteries.     

伊布利特对犬心脏窦房结和房室结的作用

目的观察伊布利特对犬心脏窦房结、房室结的影响。方法 18只成年健康雄性杂种犬,麻醉后气管插管,开胸并缝合电极,伊布利特按0.10 mg/kg静脉推注给药(10 min缓推,给药30 min后按照0.01 mg/min静脉滴注维持),观察给药前后心率、窦房结和房室结功能的变化。结果伊布利特对心率有明显的抑制作用,作用的高峰时间在给药后20～30 min,2 h后心率基本恢复到用药前的水平;1只犬在给药后出现长达5 s的窦性停搏;试验中,1只犬在给药后5 min出现房室结2:1下传,给药后20 min该现象自行消失。结论伊布利特可明显减慢窦性心率,对窦房结的自律性有一定的抑制作用,对房室结的功能也有一定的抑制作用。     

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.     

Ionic basis of ischemia-induced bradycardia in the rabbit sinoatrial node

To investigate the basis of ischemia-induced bradycardia (<60 beats/min), we isolated pacemaker cells from the rabbit sinoatrial node and exposed them to ischemic-like conditions, including omission of glucose, pH 6.6, and either 5.4 or 10 mM KCl to evaluate the role of increased serum [K]. A perforated-patch technique was employed to test the hypothesis that the arrhythmia is caused by attenuation of inward currents that contribute to the diastolic depolarization. After exposure to "ischemic" Tyrode containing 5.4 mM KCl, the pacemaker cells exhibited 13% slower beat rates and action potentials with 6-mV greater overshoots and 44% longer durations. In contrast, after exposure to "ischemic" Tyrode containing 10 mM KCl, the pacemaker cells exhibited a 7-mV depolarization of the maximum diastolic potential but no significant change in the overshoot. Beat rates were slowed by 43%, and the action potentials were prolonged by 46%. "Ischemic" Tyrode containing 5.4 mM KCl increased L-type Ca current, decreased T-type Ca current and reduced Ni-sensitive inward current tails (presumably Na-Ca exchange current), even after treatment with 40 muM ryanodine to block Ca release from the sarcoplasmic reticulum. "Ischemic" Tyrode containing 10 mM KCl increased hyperpolarization-activated inward current at diastolic potentials and reduced the slowly activating component, but not the rapidly activating component, of delayed rectifier K current. Our results suggest that reductions of inward Na-Ca exchange current and T-type Ca current contribute to "ischemia"-induced "bradycardia" in sinoatrial node pacemaker cells.     

食道电生理评估植物神经对窦房结及房室结功能的影响

目的　鉴别结内病窦综合征与结外病窦综合征。方法　对临床上疑诊为病窦综合征的３６８ 例患者用食道电生理检查，测定窦房结传导时间（ Ｓ Ａ Ｃ Ｔ）、窦房结恢复时间（ Ｓ Ｎ Ｒ Ｔ）、文氏点、２∶１阻滞点。将３６８ 例分成３ 组：正常为１ 组，结内病窦为２ 组，结外病窦组即迷走神经张力增高为３ 组。结果　１ 组与３ 组年龄相比差异不显著（ Ｐ＞ ０．０５），２ 组年龄明显大于以上两组（ Ｐ＜ ０．０１）。静脉注射阿托品前心率：１ 组＞ ３ 组＞ ２ 组； Ｓ Ａ Ｃ Ｔ、 Ｓ Ｎ Ｒ Ｔ：２ 组＞ ３ 组＞ １ 组；文氏点、２∶１ 阻滞点：３ 组＜ ２ 组＜ １ 组。静脉注射阿托品后：１ 组、３ 组各参数明显改善，３ 组各参数恢复正常。２ 组 Ｓ Ａ Ｃ Ｔ、 Ｓ Ｎ Ｒ Ｔ 仍然明显延长。房室传导功能各组间在注射阿托品后相比差异不显著（ Ｐ＞ ０．０５）。结论　１食道电生理加阿托品试验能准确鉴别结内病窦综合征和结外病窦综合征。２房室结的传导功能与窦房结功能障碍并不直接相关。迷走神经张力增高对房室结的影响更大。     

Effect of glycolytic inhibitors on the sinoatrial node,atrium and atrioventricular node in the rabbit heart

The effect of unspecific noncompetitive (iodoacetic acid; IAA) and of specific competitive (deoxyglucose) glycolytic inhibitors were studied under aerobic and anaerobic conditions in the isolated sinoatrial (SA) node, right atrium and atrioventricular (AV) node of the rabbit heart. Transmembrane action potentials were recorded simultaneously with the His bundle electrogram. Under aerobic conditions (Po₂ 460 mmHg), 7.5 × 10^?5m IAA caused no significant alterations of sinus rate, intraatrial and AV nodal conduction. Under hypoxic conditions (Po₂ 40 mmHg), 7.5 × 10^?5m IAA resulted in rapid and complete abolition of the SA and AV nodal electrical activity and in a more delayed atrial inexcitability. Similar changes were never observed in the presence of hypoxia alone. Higher concentrations of IAA (5 × 10^?4m) severely depressed the sinus rate and the AV nodal conduction already under aerobic conditions. The action potential amplitude and the rate of diastolic depolarization of the SA nodal fibers was significantly reduced, the maximum diastolic potential remained unchanged. In atrial fibers, 5 × 10^?4m IAA caused predominantly shortening of the action potential duration but had less marked and delayed depressant effects on the action potential amplitude. Electrophysiologic abnormalities included Mobitz type II sinoatrial block. The electrophysiological effects of deoxyglucose (50 mm) under aerobic and hypoxic conditions resembled those obtained with 7.5 × 10^?5m IAA. The results suggest that the “normal” nodal function is predominantly related to aerobic metabolism but that under hypoxic conditions glycolytic energy production can effectively contribute to the maintenance of nodal electrical activity. Also that the specific relation between cardiac metabolism and electrical activity of nodal and atrial cells may at least partly be explained by the particular electrical membrane properties of the various fiber types.     

The atrioventricular node: origin, development, and genetic program

The sinus node generates the electrical impulse, which spreads rapidly over both atria, causing them to contract simultaneously. In the normal heart, a layer of connective tissue electrically insulates the atria and ventricles. The only pathway that crosses this plane is the atrioventricular conduction axis, through which the impulse reaches the ventricles. Within the axis, the atrioventricular node delays the impulse, allowing the ventricles to be filled before their contraction is initiated. Moreover, the atrioventricular node protects the ventricles from rapid atrial arrhythmias and may take over pacemaker function when the sinus node fails. In pathological conditions, these complex physiological properties contribute to several types of arrhythmias that originate from the atrioventricular conduction system. One example is atrioventricular block, which requires electronic pacemaker implantation because there is currently no cure for this arrhythmia. Because conduction system defects may arise during embryonic development, the mechanisms of conduction system development have been intensively studied. Nevertheless, its developmental origin, molecular composition, and phenotype have remained fertile subjects of research and debate. Lineage and expressional analyses have indicated that the atrioventricular node develops from a subpopulation of precursor cells in the dorsal part of the embryonic atrioventricular canal. These cells become distinct early in development, are less well differentiated compared to the developing working myocardium, and, in addition to their cardiogenic gene program, activate and maintain a neurogenic gene program.     

Effect of hypoxia on the sinoatrial node, atrium, and atrioventricular node in the rabbit heart.

We used intracellular microelectrodes to study the effects of hypoxia on the isolated, superfused sinoatrial (SA) node, atrium, and atrioventricular (AV) node of the rabbit heart. Hypoxia decreased the rate of spontaneous impulse initiation in SA nodal fibers by decreasing the slope of diastolic depolarization. With gradually decreasing Po2, the sinus rate was reduced; concomitantly, the corrected sinus node recovery time after rapid atrial stimulation was much less affected demonstrating marked prolongation only under severe anoxic conditions. Hypoxia decreased the amplitude of action potentials of the SA node and of the AV node but not of the atrium. SA and AV nodal conduction were slowed by hypoxia; intraatrial conduction was not significantly affected. AV nodal conduction block occurred at lower atrial rates, and the effective refractory period of the AV node was prolonged. Inhomogeneity of SA and AV nodal impulse propagation often was observed in the presence of hypoxia. This was associated with concealed reentry within both nodal areas. The extracellular K+ concentration of the atrial tissue was measured with ion-sensitive microelectrodes. [K+]o remained unchanged even after prolonged periods of severe hypoxia. These results are consistent with the hypothesis that acute hypoxia predominantly inhibits slow response activity but has only little effect on the fast inward sodium current.     

Electrophysiological effects of different dosage of adenosine triphosphate on normal sinoatrial and atrioventricular node]

In order to study the electrophysiological basis of smaller dosage that would terminate PSVT effectively and decrease side effects remarkably, we have observed the electrophysiological effects of ATP in different dosage (5mg, 10mg, 15mg) on the sino-atrial node (SAN) and atrioventricular node (AVN). Cardiac electrophysiological investigations were carried out in 62 patients with history of PSVT by using the method of trans-esophagus ECG and body surface ECG continuously and simultaneously, during the normal sinus rhythm and PSVT. The results showed that when the effect of 10mg ATP on SAN was not clinically significant yet, it did strikingly block the AVN conduction enough to terminate the PSVT with no severe arrhythmias. 37 cases of 62 patients were provoked PSVT during control electrophysiological study, the PSVTs of 33 cases out of these 37 patients (89.7%) were terminated by using 10mg ATP. There was no serious bradyarrhythmias after PSVT termination. We suggest that 10mg ATP is a reliable dose for PSVT termination.     

动态心电图等三种方法对窦房结及房室结功能诊断价值的再探讨

目的 再评估动态心电图、阿托品试验及其前后食管调搏检测对窦房结及／或房室结功能的诊断价值。方法 观察35例经动态心电图检查符合病态窦房结综合征的上述检查结果。结果 7例食管调搏正常及阿托品试验阴性;6例阿托品试验阳性,其前后食管调搏均异常;17例阿托品试验前食管调搏异常,阿托品试验后恢复正常。结论 以上检查对诊断窦房结及／或房室结功能障碍各有不同的意义,应绫合应用以提高正常诊断率。     

Origin of the sinoatrial node and atrioventricular node arteries in right, mixed, and left inferior emphasis systems.

The origin of the sinoatrial node artery (SAN) and atrioventricular node artery (AVN) was determined for 118 patients with normal coronary arteriograms. The coronary arteriograms of the 118 patients were divided into right (66.1%), mixed (26.3%), and left (7.6%) inferior emphasis systems. The SAN arose from the right coronary artery in 53%, the left coronary artery in 35%, and had a dual origin in 11%. The proximal right coronary artery was the origin of the SAN in 48.7% of right, 60.5% of mixed, and 55.6% of left inferior emphasis systems. The left coronary artery was the origin of the SAN in 38.5% of right, 25.8% of mixed, and 44.4% of left inferior emphasis systems. The AVN arose from the right coronary artery in 84%, the left coronary artery in 8%, and from both in 8% of the 118 patients. The right coronary artery was the origin of the AVN in 98.7% of right, 74.2% of mixed, and 0% of left inferior emphasis systems. The left coronary artery was the origin of the AVN in 0% of right, 25.8% of mixed, and 100% of left inferior emphasis systems.     

Familial sinoatrial node dysfunction. Increased vagal tone a possible aetiology.

Clinical and electrophysiological studies of a 13-year-old boy with sinus bradycardia revealed sinus node dysfunction. Long-term follow-up data of members of his family indicated familial sinus node dysfucntion. Increased vagal tone was present in all patients. It is suggested that excessive vagal discharge for a pronlonged time may be the basic mechanism of sinus node dysfunction in these patients.