Neural Regulation of Atrioventricular Conduction

Irisawa, Hiroshi; Caldwell, W.M.; Wilson, M F

doi:10.2170/jjphysiol.21.15

Cited by 37 publications

(21 citation statements)

References 17 publications

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“…Right sided cardiac sympathetic projections exert more pronounced effects on heart rate than left sided projections do (2-4), whereas left sided sympathetic inputs predominantly modulate AV conduction (5,7,8,23), but right sided sympathetic inputs also modulate AV conduction consistently (1,7). We stimu lated the intracardiac sympathetic nerves to the AV nodal region at the fatty tissue of the junction of the inferior vena cava and left atrium, and this stimulation activates at least a part of the ventrolateral cardiac nerves from the left ansa subclavia (11).…”

Section: Discussionmentioning

confidence: 99%

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Differential intracardiac sympathetic and parasympathetic innervation to the SA and AV nodes in anesthetized dog hearts.

Furukawa¹,

Narita²,

Takei³

et al. 1991

Jpn.J.Pharmacol

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Stimulation of discrete intracardiac sympathetic nerves to the SA (SAS stimulation) or AV nodal region (AVS stimulation) increased the heart rate or de creased AV conduction time and caused an AV junctional rhythm, respectively, in anesthetized dogs treated with atropine. Topical application of tetrodotoxin (TTX) at the SAS or AVS stimulation locus totally inhibited the response to each stimulation, whereas each TTX treatment slightly attenuated the chronotropic response to the right ansa stimulation by 23 ± 7.7% and the dromotropic response to the left ansa stimula tion by 7 ± 7.5%. TTX abolished AVS stimulation-induced one. Before atropine, topical application of hexamethonium at the locus for stimulation of intracardiac para sympathetic nerves to the SA (SAP stimulation) or AV nodal region (AVP stimula tion) abolished almost totally negative chronotropic responses to SAP and cervi cal vagus stimulation or negative dromotropic responses to AVP and cervical vagus sti mulation, respectively. These results demonstrate that activation of a very small population of intracardiac sympathetic nerves to target cells is enough to induce posi tive chronotropic and dromotropic responses in the heart in situ, and that SA and AV nodal pacemaker activity and AV conductivity are controlled multi-directionally by in tracardiac sympathetic nerves in contrast with parasympathetic ones.Activation of both right and left sympathetic nerves to the heart increases heart rate, short ens atrioventricular (AV) conduction time (AVCT), and increases myocardial contractile force (1, 2). Right sided sympathetic projec tions exert more pronounced effects on rate (2-4), whereas left sided sympathetic projec tions predominantly modulate AV conduction (5-8). The more peripherally located the point of electrical activation of cardiac sym pathetic nerves, the more distinct the effects on control of regional cardiac function (2, 9). Projections of extracardiac sympathetic effer ents to automatic, conductile and contractile tissues of the dog heart are parallel, but dis tinct (10). Recently, we have found that sti mulation of the intracardiac sympathetic nerve fibers to the SA (SAS stimulation) and AV nodal regions (AVS stimulation) results in selective positive chronotropic and dromotro pic responses, respectively, in the atropine treated dog heart (11). There are loci for SAS and AVS stimulation, i.e., the right atrial side of junctions of the right pulmonary veins and

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Section: Discussionmentioning

confidence: 99%

“…Right sided sympathetic projec tions exert more pronounced effects on rate (2-4), whereas left sided sympathetic projec tions predominantly modulate AV conduction (5)(6)(7)(8). The more peripherally located the point of electrical activation of cardiac sym pathetic nerves, the more distinct the effects on control of regional cardiac function (2,9).…”

mentioning

confidence: 99%

Differential intracardiac sympathetic and parasympathetic innervation to the SA and AV nodes in anesthetized dog hearts.

Furukawa¹,

Narita²,

Takei³

et al. 1991

Jpn.J.Pharmacol

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“…12 Others have reported, however, that at submaximal stimulation levels, the right and left vagi produce an equal prolongation of AV conduction time.…”

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confidence: 97%

The influence of the parasympathetic nervous system on atrioventricular conduction.

Martin¹

1977

Circulation Research

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IN THIS brief review I will attempt to amalgamate current findings with important historical concepts about the influence of the parasympathetic nervous system on atrioventricular (AV) conduction. I first will describe the innervation of the AV nodal region. Then I will discuss the influence of acetylcholine and associated cholinergic agents, the effects of vagal stimulation, and the role of the vagus in the genesis of arrhythmias. Finally, I will describe briefly certain cardiovascular reflexes that affect AV conduction. I have not attempted to provide an exhaustive list of references; rather, the most relevant works were arbitrarily selected to illustrate specific points. I regret that many worthy contributions had to be omitted. Innervation of the AV NodeIt has been known since the early part of this century that the autonomic nervous system can affect AV conduction profoundly. "3 Anatomical studies during this era revealed that the AV node is richly innervated 4 -5 and that the density of nerve fibers in this region exceeds that in the myocardium. 6 In subsequent years, it was found that ganglia, nerve fibers, and nerve nets lie in close proximity to the AV node in the human heart 7 and that the terminations on nodal tissue vary from fine fibrils to complex reticular nets.8 It should be noted, however, that all of these early works were based upon light microscopy and variable staining techniques and, thus, not all of these results were accepted conclusively.Most of the definitive work in this area has been done within the past 10-20 years. I first will review the neural pathways to the AV node, and then describe the terminal innervation of the node. Although the focus here is on the vagus, the adrenergic innervation will also be mentioned briefly for completeness.Geis et al. 9 recently have delineated the various autonomic pathways to the AV node of the dog. They found that the left anterior limb of the ansa subclavia and the ventrolateral cardiac nerves innervated the AV node in each dog studied. The posterior ansa on the left side and both limbs of the ansa on the right side innervated the A V node in one-half to two-thirds of their dogs, whereas the innominate, the recurrent cardiac, the craniovagal, and the ventromedial cardiac nerves innervated the AV node in less than one-fourth of the animals. The right-sided sympathetic innervation of the AV node consisted of nerve fibers that accompanied the great vessels to the region where the inferior vena cava approximates the inferior border of the left atrium. The sympathetic innervation on the left side followed similar pathways, but additional fibers reached the node through the ventrolateral cardiac nerve. Both the left and right parasympathetic innervations traversed pathways along the superior left atrium and the region where the inferior vena cava lies close to the inferior margin of the left atrium.Thus it has been demonstrated that nerve fibers from both sides of both autonomic divisions project onto the AV node. The differential effects of neural act...

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“…The increased AV interval was caused by prolongation of the AH interval (fig. 2); the HV interval remained unchanged (20 tropic and dromotropic changes was confirmed in patient 2 ( fig. 3).…”

Section: Methodsmentioning

confidence: 69%

Prolongation of atrioventricular conduction time by electrical stimulation of the carotid sinus nerves in man.

Borst

Karemaker²,

Dunning³

1982

Circulation

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SUMMARY Electrical stimulation of the carotid sinus nerves was applied during diagnostic catheterization of two patients who had coronary artery disease. The immediate reflex prolongation of the atrioventricular (AV) interval was due to prolongation of the AH interval only and was roughly parallel to the reflex RRAinterval prolongation evoked without atrial pacing. After cholinergic block, the reduced prolongation of both the RR interval and the AV interval caused by reflex inhibition of sympathetic tone followed a time course similar to the arterial pressure decrease. This is the first demonstration in man of the parallel baroreflex effects on the sinoatrial node and the AV node.THE NEGATIVE chronotropic effect of increased arterial baroreceptor activity has been well documented in animals1 and in man.2-5 Much less information is available on baroreflex control of atrioventricular (AV) conduction." We are not aware of any report on the time course of AV conduction changes in man evoked by the abrupt increase and decrease of baroreceptor afferent activity.We describe here the reflex effects on AV conduction time evoked by electrical stimulation of the carotid sinus nerves (CSN) during atrial pacing (with His-bundle recording in one case).7 Methods Two patients with coronary heart disease were studied after informed consent during diagnostic cardiac catheterization. Patient 1 was 57 years old and patient 2 was 65 years old. Patient was reexamined 3 years later to exclude the existence of cardiac conduction defects. The techniques for right atrial pacing and for recording His-bundle activity, ECG and brachial artery pressure have been described.8' ' The subjects were in stable condition without signs of cardiac failure. No ,B-blocking drugs were used at the time of the study. In one patient, atropine, 0.04 mg/kg, was administered to block vagal control of the heart. This patient had first-degree AV block.The studies were performed at least 20 months after implantation of the receiver-electrodes assembly of the CSN stimulator (Angistat, Medtronic). Therapeutic application of CSN stimulation has been fully described elsewhere.8" 10,11 A modified7 12 stimulator produced 0. pulses for periods of 15-90 seconds. The stimulator was switched on or off by the QRS complex of the ECG. The stimulus frequency was 80-120 Hz12 and the estimated intensity was < 2.5 V; the exact voltage is unknown due to the nature of the device.7In patients with coronary heart disease, the therapeutically adequate stimulus intensity (used in this study) remains below the threshold for activation of chemoreceptor fibers, as judged from the absence of changes in respiratory rate or minute volume.7 8All signals were monitored on an instrumentation recorder and analyzed later with the help of a digital computer. AV conduction time was defined as the AV interval between the onset of the pacing stimulus artifact and the peak of the R wave or S wave in the ECG. We determined the mean arterial pressure by electronic low-pass filtering the phasic signal ...

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Neural Regulation of Atrioventricular Conduction

Cited by 37 publications

References 17 publications

Differential intracardiac sympathetic and parasympathetic innervation to the SA and AV nodes in anesthetized dog hearts.

Differential intracardiac sympathetic and parasympathetic innervation to the SA and AV nodes in anesthetized dog hearts.

The influence of the parasympathetic nervous system on atrioventricular conduction.

Prolongation of atrioventricular conduction time by electrical stimulation of the carotid sinus nerves in man.

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