Disease relevance of Sinoatrial Node

• Calcium-channel blocking agents and, less commonly, digoxin may perpetuate the duration of paroxysmal atrial fibrillation, and virtually all agents can cause sinus node dysfunction or atrioventricular block [1].
• After vagal section or muscarinic receptor blockade, however, adenosine injection causes bradycardia via a direct sinoatrial node inhibition [2].
• Adenosine terminated sinus node reentrant tachycardia in 6 of 6 patients and terminated atrial tachycardia due to triggered activity in the 1 patient in whom it was identified [3].
• The results indicate that in addition to the direct effects of thyroid hormone on sinus node automaticity there is an abnormality in parasympathetic control of heart rate in hyperthyroidism [4].
• In this study, we analyzed patients suffering from sinus node dysfunction, progressive cardiac conduction disease, and idiopathic ventricular fibrillation for mutations in HCN4 [5].

Psychiatry related information on Sinoatrial Node

• In conclusion, in patients with NSNF propafenone 1. does not affect sinus node automatism and 2. prolongs significantly DSACT, which, however, remains within the upper normal limit [6].

High impact information on Sinoatrial Node

• Cimetidine and sinus-node function [7].
• Reversible sinus-node abnormalities due to lithium carbonate therapy [8].
• Sinus node dysfunction caused by methyldopa and digoxin [9].
• In contrast, FHC mice demonstrated (a) electrocardiographic abnormalities including prolonged repolarization intervals and rightward axis; (b) electrophysiological abnormalities including heterogeneous ventricular conduction properties and prolonged sinus node recovery time; and (c) inducible ventricular ectopy [10].
• Amiodarone had no significant effect on sinus node response to either stellate stimulation or intranodal administration of norepinephrine [11].

Chemical compound and disease context of Sinoatrial Node

• BACKGROUND: Low-dose atropine causes bradycardia either by acting on the sinoatrial node or by its effects on central muscarinic receptors increasing vagal activity [12].
• Propranolol may cause marked bradyarrhythmias in some patients with sinus node dysfunction, and should be used with caution in these patients [13].
• In the absence of cardiac glycoside, the only demonstrable abnormalities of sinus node function were mild resting sinus bradycardia and failure to respond to atropine administration [14].
• Relative contraindications to the use of verapamil include left ventricular dysfunction and sinus node and atrioventricular conduction disease [15].
• In therapeutic doses, lithium produces reversible T wave flattening and inversion in the electrocardiogram: rarely, it may cause sinus node dysfunction or ventricular arrhythmias [16].

Biological context of Sinoatrial Node

• Furthermore, the reduction in heart rate in these animals provides support for a direct depressant effect of quinidine on the sinus node [17].
• The objectives of the present study were to determine whether Cx43 is expressed by sinus node myocytes, to characterize the spectrum of connexin expression phenotypes in sinus node pacemaker cells, and to define the spatial distribution of different connexin phenotypes in the intact sinus node [18].
• Addition of zatebradine, a direct sinus node inhibitor, provides no greater exercise tolerance benefit in patients with angina taking extended-release nifedipine: results of a multicenter, randomized, double-blind, placebo-controlled, parallel-group study. The Zatebradine Study Group [19].
• In a study of the electrophysiological effects of alinidine a concentration of 0.7-14.3 mumol X litre-1 decreased the rate of diastolic depolarisation and prolonged especially the terminal part of the action potential in the rabbit sinoatrial node [20].
• 3. When membrane potential recordings were made from sino-atrial node cells, in which beating had been abolished by adding the organic calcium antagonist nifedipine, sympathetic nerve stimulation initiated excitatory junction potentials (EJPs) which had time courses similar to those of the tachycardias recorded from beating preparations [21].

Anatomical context of Sinoatrial Node

• Amiodarone was selectively perfused into the sinus node artery and atrioventricular node artery of 51 dogs [11].
• METHODS: Light microscopic examination of subserial sections of the sinus node, atrioventricular node and His bundle, coronary chemoreceptor and regional nerves, ganglia, and small coronary arteries [22].
• In the right atrium, 3 HNK-1-positive connections were demonstrated between the sinoatrial node and the right atrioventricular ring [23].
• METHODS AND RESULTS: We used standard electrophysiological techniques to study the effects of PTH and PTHrP on isolated rabbit sinus node, isolated canine Purkinje fibers, and disaggregated rabbit sinus node myocytes [24].
• Autoradiographic inhibition curves with betaxolol or ICI-118,551 demonstrated that both the sinoatrial node and the atrioventricular bundle had inhibition profiles similar to the surrounding myocytes (predominantly beta 1) but unlike the inhibition profiles of arterioles (predominantly beta 2) [25].

Associations of Sinoatrial Node with chemical compounds

• Acute effects of amiodarone upon the canine sinus node and atrioventricular junctional region [11].
• The electrophysiological effects of ouabain on sinus node and atrium in man [26].
• Adverse cardiac reactions (proarrhythmia or sinus node suppression) attributable to flecainide occurred in 11 of 63 patients (17%); in 9 (82%) of these 11 patients, events were detected during either in-hospital monitoring or the electrophysiologic study done before discharge [27].
• Twenty other patients with sinus node disease underwent electrophysiologic studies both before and after i.v. administration of 0.04 mg of atropine alone [28].
• At a mean dose of 179 +/- 88 micrograms/kg (+/- SD), adenosine suppressed sinus node automaticity and depressed atrioventricular (AV) nodal conduction [29].

Gene context of Sinoatrial Node

• The pacemaker channels HCN2 and HCN4 have been identified in cardiac sino-atrial node cells [30].
• Throughout cardiac development, Tbx3 is expressed in an uninterrupted myocardial domain that extends from the sinoatrial node to the atrioventricular region [31].
• Consistent with this is the recent description of KCNE2, which is highly expressed in the sinoatrial node, as a beta-subunit of rapidly activating HCN1 and HCN2 channels [32].
• Sinus node recovery times after carbachol and sinus cycle lengths were shorter and ventricular effective refractory periods were greater in KO mice than in WT mice [33].
• Functional alterations in the SAN following heterozygous-targeted disruption of Scn5a thus closely resemble those observed in clinical sinus node dysfunction [34].

Analytical, diagnostic and therapeutic context of Sinoatrial Node

• To determine the contribution of disopyramide's suggested opposing direct depressant and indirect acceleratory actions on sinus node function, we studied the effects of disopyramide, 1 x 10(-7) to 1 x 10(-4) M, on isolated rabbit sinus node preparations using standard microelectrode techniques [35].
• ECG responses to isoproterenol are also similar in the 2 groups. beta-Galactosidase staining in postnatal minK (-/-) hearts is highly restricted, to the sinus-node region, caudal atrial septum, and proximal conducting system [36].
• The direct and indirect chronotropic effects of clonidine (0.001--10 micrograms/ml) were studied by selective perfusion of the sinus node artery of 20 pentobarbital anesthetized dogs [37].
• 1. The effect of the bradycardic agent S 16257 on the main ionic mechanisms of diastolic depolarization in sinoatrial node cells isolated from rabbit heart, was investigated by the patch-clamp technique in whole-cell and macro-patch recordings [38].
• Administration of PGI2 either to the donor dog or directly into the sinus node arterial cannula did not alter the atrial rate or developed tension in the isolated blood perfused atrial preparation [39].

References