[Automation of the sinoatrial node and sinoatrial conduction and the autonomic nervous system].
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Autonomic Nervous System↗
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[Changes in the automatism of the sinoatrial node and sinoatrial conduction in patients with paroxysmal forms of atrial fibrillation].
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Adult↗
[Study of post-stimulation depression of the sinoatrial node and sinoatrial conduction time by means of atrial electric stimulation in patients with normal sinus rhythm].
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Action Potentials↗
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.
Action Potentials↗
Distribution of atrial and nodal cells within the rabbit sinoatrial node: models of sinoatrial transition.
BACKGROUND: In the sinoatrial node (SAN) the course of the action potential gradually changes from the primary pacemaker region toward the atrium. It is not known whether this gradient results from different intrinsic characteristics of the nodal cells, from an increasing electrotonic interaction with the atrium, or from both. Therefore we have characterized the immunohistochemical, morphological, and electrophysiological correlates of this functional gradient. METHODS AND RESULTS: The distribution of rabbit nodal myocytes in the SAN has been studied by immunohistochemistry. After cell isolation, the electrophysiological characteristics of different nodal cell types were measured. (1) The staining pattern of a neurofilament protein coincides with the electrophysiologically mapped pacemaker region in the SAN. (2) Enzymatic digestion of the SAN reveals three morphologically different nodal cell types and one atrial type. Of each nodal cell type, neurofilament-positive as well as neurofilament-negative myocytes are found. Atrial cells are all neurofilament-negative. (3) In contrast to previous findings, we observed atrial cells in the very center of the SAN. The relative number of atrial cells gradually increases from the central pacemaker area toward the atrium. (4) Differences in electrophysiological characteristics between individual nodal cells are not associated with differences in cell type. CONCLUSIONS: (1) The expression of neurofilaments can be used to delineate the nodal area in the intact SAN but is not sufficiently sensitive for characterizing all individual isolated nodal cells. (2) A fundamentally different organization of the SAN is presented: The gradual increase in density of atrial cells from the dominant area toward the crista terminalis in the SAN causes a gradual increase of atrial electrotonic influence that may be an important cause of the gradual transition of the nodal to the atrial type of action potential.
Action Potentials↗
[Experimental studies on atrial fibrillation. On the significance of the sinoatrial node and specialized conducting system from the sinoatrial node to the left atrium as to occurrence and maintenance of aconitine fibrillation].
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Aconitum↗
The surgical anatomy of the sinoatrial node.
The sinoatrial nodes (SAN) were observed, dissected, and measured on 95 adults and 30 child hearts under a dissection microscope. The majority of the SANs in adults are characterized by their pale color, firm consistency, and the location in relation to the penetration of the SAN artery, and they can be located in the superior part of the terminal sulcus. The SANs in children, however, are not easily discerned. The variation of the apex of the right auricular crest and the notch in the superior part of the terminal sulcus have been described, and the present authors suggested that the trigone of the SAN could be used as an important landmark to identify the SAN. The surface features on the SAN, its relationship to the surrounding myocardium and its surgical significance during operation are further discussed.
Adult↗
The mammalian sinoatrial node.
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.
Animals↗
Functional and morphological organization of the cat sinoatrial node.
The feline sinoatrial node has a unifocal impulse generation as previously described for rodents. Its main component is collagen. The primary pacemaker consists of at most 2000 cells, but appears to function normally with less than 500 cells. Primary pacemaker cells are found in the area where empty cells are predominant. A negative correlation between myofilament density and diastolic depolarization rate, known to exist in the rabbit and guinea-pig, is absent in the cat. Gap junctions are seen in the center and in the periphery of the nodal region, but they are extremely rare. The electrophysiological characteristics of the primary pacemaker of the cat are quite similar to those of the rabbit, although the nodal morphology is very different. Abrupt transitions from one cell type into another are observed in the feline sinoatrial node. From this morphological point of view the feline sinoatrial node resembles the canine and human sinoatrial nodes more than the lapine sinoatrial node.
Animals↗
Presence or absence of glycogen-beta particles in sinoatrial node cells.
The sinoatrial node is formed by specialized cells, the main ultrastructural differences of which, as compared with ordinary atrial myocardium, are a pale cytoplasm and sparse myofibrils. Moreover, nodal cells have been described to contain large amounts of glycogen particles in their pale cytosol; these glycogen inclusions are often used as the main criterion for identifying nodal cells. Nevertheless, the presence of glycogen cytosolic inclusions has been discussed by several authors. This paradox was solved by the description of some undesirable effects of uranyl acetate when used en bloc. To prove the presence of glycogen granules in nodal cells and the effects of uranyl acetate en bloc, we performed an ultrastructural study of the sinoatrial node in rats of different ages using different staining techniques. Our results do not reveal any beta-particles in nodal cells in tissues processed by either general or glycogen-specific methods. Uranyl acetate staining did not cause any change of appearance in the nodal or ordinary myocardium. From these results, one could conclude that, on the one hand, sinoatrial nodal cells do not show deposits of beta-particles of glycogen which can be detected with ultrastructural techniques, and, on the other hand, that uranyl acetate does not cause any morphological artifacts.
Aging↗
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.
Actin Cytoskeleton↗
Ageing-related changes of connexins and conduction within the sinoatrial node.
Clinical studies have shown that sinoatrial node dysfunction occurs at the highest incidence in the elderly population. Guinea-pigs were studied throughout their lifespan (i.e. birth to 38 months) to investigate the possible mechanism leading to nodal dysfunction. Using immunofluorescence with confocal microscopy, Cx43 protein expression was shown at birth to be present throughout the sinoatrial node and atrial muscle, however, at one month Cx43 protein was not expressed in the centre of the sinoatrial node. Throughout the remainder of the animal's lifespan the area of tissue lacking Cx43 protein progressively increased. Western blot provided verification by quantitative analysis that Cx43 protein expression within the sinoatrial node decreased with age; however, the expression of other cardiac connexins, Cx40 and Cx45, did not differ with age. Analysis of conduction maps showing propagation of the action potential across the sinoatrial node, from the initiation point to the crista terminalis, found that the action potential conduction time taken and conduction distance increased proportionally with age; conversely the conduction velocity decreased with age. We have shown ageing induces degenerative changes in action potential conduction, contributed to by the observed loss of Cx43 protein. Our data identify Cx43 as a potential therapeutic target for quashing the age-related deterioration of the cardiac pacemaker.
Action Potentials↗
The pacemaker cell of the sinoatrial node of the rabbit.
Rabbit sinoatrial nodes were isolated and studied in an attempt to determine the cell of origin of the true pacemaker potential. Cells of the sinoatrial node of the rabbit giving rise to the characteristic true pacemaker potential were iontophoretically tagged with lanthanum. The lanthanum appeared within the cytoplasm of cells, which morpholigically are "P" cells. The lanthanum appeared as small, amorphous, electron-dense globules. It is concluded from this study that the P or pale cell is the source of the true pacemaker action potential of the sinoatrial node.
Action Potentials↗
[Direct recording of the electrical activity of the sinoatrial node].
The electrical activity of the sinoatrial node was recorded simultaneously from the epicardial and endocardial surfaces of the sinoatrial node in 73 dogs. The electrical activity of sinoatrial node had the form of a slow deflection and a rapid preatrial deflection, the duration of the former being 81 +/- 28 msec and reflecting slow propagation of excitation within the sinus node. Duration of the rapid preatrial deflection was 17 +/- 11 msec. It reflects the rapid propagation of the sinus impulse (probably, the rapid spread of the excitation in corona of the sinus node and invasion in crista terminals). The form and duration of the slow and rapid deflections changed under the influence of drugs.
Adrenergic beta-Antagonists↗
On the mechanisms of cholinergic control of the sinoatrial node discharge.
It has been proposed that cholinergic agonists inhibit the sinoatrial node discharge by shifting the activation range of the hyperpolarization-activated inward current If to more negative values or by increasing potassium conductance. In the former instance, cesium will potentiate the cholinergic inhibition by blocking any residual If; in the latter instance, Cs+ and Ba2+ will antagonize the inhibitory action by blocking K+ channels. The changes in discharge induced by high and low concentrations of carbachol were studied using an electrophysiologic technique in isolated guinea pig sinoatrial node perfused in vitro in the absence and presence of different concentrations of Cs+ and Ba2+. In Tyrode solution, high carbachol concentrations (0.5-2 microM) slowed the sinoatrial node by hyperpolarizing the membrane and by reducing the amplitude of diastolic depolarization; and stopped the sinoatrial node by preventing the attainment of threshold potential. Adding Cs+ (10 mM) to carbachol increased the rate in slowly discharging sinoatrial node and induced spontaneous discharge in quiescent sinoatrial node. In high [K+]o (approximately 12 mM), carbachol slowed or stopped the slow responses and adding Cs+ accelerated or induced discharge. Both in Tyode and in high [K+]o, in the presence of Cs+, carbachol did stop the sinoatrial node. In the presence of carbachol, Ba2+ (0.1 mM) accelerated or induced discharge, as Cs+ did. Atropine (1 microM) prevented both the slowing or suppression by carbachol and the acceleration of sinoatrial node by Cs+ in the presence of carbachol. Low carbachol concentrations (0.05-0.1 microM) decreased the rate to a similar extent in the absence and the presence of a low concentration of Cs+ (2 mM, which blocks If but not K+ channels), but markedly less in the presence of 0.5-0.75 mM Ba2+ (which block K+ channels but not If). We conclude that cholinergic agonists slow or stop the sinoatrial node by a shifting the membrane potential toward the more negative subsidiary pacemaker range and away from the threshold. The results with Cs+ and Ba2+ indicate that both high and low concentrations of carbachol decrease sinoatrial node discharge by activating the I(K,ACh) channels rather than by decreasing If.
Animals↗
Catheter ablation of sinoatrial node reentrant tachycardia.
OBJECTIVES: This study evaluates 1) the safety and efficacy of catheter delivery of radiofrequency current to eliminate sustained sinoatrial node reentrant tachycardia; 2) the incidence of sinoatrial node reentrant tachycardia in the current group of patients undergoing electrophysiologic study for paroxysmal supraventricular tachycardia; and 3) the association of sinoatrial node reentrant tachycardia with other tachyarrhythmias. BACKGROUND: Sustained sinoatrial node reentrant tachycardia is an uncommon cause of paroxysmal supraventricular tachycardia that is reported to occur infrequently in conjunction with other arrhythmias. Although pharmacologic and surgical therapies are available, there is limited information with regard to catheter ablation of sinoatrial node reentrant tachycardia. METHODS: Ten patients with sustained sinoatrial node reentrant tachycardia underwent electrophysiologic study and radiofrequency current ablation. Patients were followed up for 9.2 +/- 6.0 months. RESULTS: Of 343 consecutive patients referred for electrophysiologic evaluation of paroxysmal supraventricular tachycardia, 11 (3.2%) were found to have inducible sustained sinoatrial node reentrant tachycardia. Nine of the 11 patients had other associated arrhythmias, including atrioventricular (AV) node reentrant tachycardia (6 patients), AV reciprocating tachycardia (2 patients), ectopic atrial tachycardia (2 patients) and bundle branch reentrant tachycardia (1 patient). In 10 patients, direct ablation of sinoatrial node reentrant tachycardia was attempted and was successful in all (confidence interval for failure 0-0.26). Sinoatrial node reentrant tachycardia was eliminated with a median of four radiofrequency current applications (range 1 to 10) at 20 to 30 W. Successful ablation site characteristics during sinoatrial node reentrant tachycardia included 1) atrial activation > or = 35 ms (mean 44 +/- 8 ms) before the onset of the surface P wave, 2) atrial activation > or = 20 ms (mean 28 +/- 6 ms) before the onset of high right atrial activation, and 3) significantly prolonged and fractionated electrograms (mean duration 87 +/- 21 ms). No complications were encountered, and there have been no recurrences of sinoatrial node reentrant tachycardia. CONCLUSIONS: Sinoatrial node reentrant tachycardia may be effectively and safely treated with radiofrequency current ablation at the site of earliest atrial activation.
Adult↗
Heterogeneous expression of the delayed-rectifier K+ currents i(K,r) and i(K,s) in rabbit sinoatrial node cells.
1. The electrical activity of sinoatrial node cells is heterogeneous. To understand the reasons for this, the density of the delayed-rectifier K+ current and its two components, i(K,r) and i(K,s), as a function of the size (as measured by cell capacitance) of rabbit sinoatrial node cells was investigated using the whole-cell voltage-clamp technique at 35 degrees C. 2. i(K,r) and i(K,s) were isolated using E-4031 and 293B. Features of the E-4031-sensitive and 293B-insensitive currents corresponded well to those of i(K,r), while features of the E-4031-insensitive and 293B-sensitive currents corresponded well to those of i(K,s). 3. The densities of the outward current under control conditions and the drug-sensitive and -insensitive currents were significantly (P < 0.01) correlated with cell capacitance, with current densities being greater in larger cells. 4. The effects of partial blockade of i(K,r) by 0.1 microM E-4031 on spontaneous action potentials were greater in smaller cells. 5. It is concluded that there are cell size-dependent differences in the density of the i(K,r) and i(K,s) components, and these may be involved in the heterogeneity of the electrical activity of single sinoatrial node cells as well as that of the intact sinoatrial node.
Action Potentials↗
[The effect of aminophylline on the sinoatrial node].
The objective of the submitted prospective study was to assess the influence of intravenously administered aminophylline on the sinoatrial node. The authors examined by electrophysiological methods 20 patients (16 without dysfunction of the sinoatrial node and 4 with dysfunction of the sinoatrial node). From the investigation patients were eliminated with an apparent and obvious cause of elevated uric acid serum levels and patients where on electrophysiological examination limited values of the corrected recovery time of the sinoatrial node were found (from 650 ms to 999 ms). To all 20 patients 240 mg aminophylline were administered by the i.v. route with in 2 mins. The following parameters were recorded: age, serum level of uric acid, basal heart rate in ms, corrected recovery time of the sinoatrial node in ms, heart rate and corrected recovery time of the sinoatrial node 5 min after completed administration of aminohpylline in ms. As regards age and uric acid serum levels there was no significant difference between dysfunction of the sinoatrial node and normal function of the sinoatrial node. Intravenously administered aminophylline hastened significantly the heart rate in patients without dysfunction of the sinoatrial node (p < 0.05). The value of the corrected recovery time of the sinoatrial node was shorter but the difference was not statistically significant. In patients with dysfunction of the sinoatrial node aminophylline did not affect the heart rate and corrected recovery time of the sinoatrial node.
Adult↗