Patterns of Sympathetic Nerve Projections onto the Canine Heart

Randall, Walter C.; Szentiványi, M.; Pace, John B.; Wechsler, J; Kaye, Michael P.

doi:10.1161/01.res.22.3.315

Cited by 111 publications

(51 citation statements)

References 6 publications

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“…We obtained the positive chronotropic and dro motropic responses to discrete intracardiac sympathetic nerve stimulation independently (11). On the other hand, an excitation of the extracardiac individual nerve trunks in the car diac plexus induces discrete responses in local ized regions of the heart (4,29,30). After se quential dissection around the major cardiac vessels of the dog heart, the resulting deficits in the responses to ansa subclavia stimulation indicate that parallel, but distinct, sympathetic efferent fibers project to the automatic, con ductile, and contractile tissues (10).…”

Section: Discussionmentioning

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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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%

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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“…3) MI animals underwent the infarction procedure described above. 4) The 90-s group was included to provide an appropriate sham operation to control for nerve injury during the ligation procedure, because cardiac nerve bundles run along major arteries and ligation of the LAD may crush nerve bundles from both stellate ganglia (27). These animals were subjected to thoracotomy and tightening of the LAD ligature for 90 s and then reperfusion and closure of the incision.…”

Section: Induction Of Infarctionmentioning

confidence: 99%

Infarction alters both the distribution and noradrenergic properties of cardiac sympathetic neurons

Li¹,

Knowlton²,

Winkle³

et al. 2004

American Journal of Physiology-Heart and Circulatory Physiology

105

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Regional changes occur in the sympathetic innervation of the heart after myocardial infarction (MI), including loss of norepinephrine (NE) uptake and depletion of neuronal NE. This apparent denervation is accompanied by increased cardiac NE spillover. One potential explanation for these apparently contradictory findings is that the sympathetic neurons innervating the heart are exposed to environmental stimuli that alter neuronal function. To understand the changes that occur in the innervation of the heart after MI, immunohistochemical, biochemical, and molecular analyses were carried out in the heart and stellate ganglia of control and MI rats. Immunohistochemistry with panneuronal markers revealed extensive denervation in the left ventricle (LV) below the infarct, but sympathetic nerve fibers were retained in the base of the heart. Western blot analysis revealed that tyrosine hydroxylase (TH) expression (normalized to a panneuronal marker) was increased significantly in the base of the heart and in the stellate ganglia but decreased in the LV below the MI. NE transporter (NET) binding sites, normalized to total protein, were unchanged, except in the LV, where [3 H]nisoxetine binding was decreased. TH mRNA was increased significantly in the left and right stellate ganglia after MI, while NET mRNA was not. In the base of the heart, increased TH coupled with no change in NET may explain the increase in extracellular NE observed after MI. Coupled with substantial denervation in the LV, these changes likely contribute to the onset of cardiac arrhythmias. tyrosine hydroxylase; norepinephrine transporter; myocardial infarction THE CARDIAC SYMPATHETIC INNERVATION travels from the base to the apex of the heart, and cardiac sympathetic function is altered in a region-specific manner after myocardial infarction (MI). Noradrenergic transmission is retained in the heart basal to the coronary ligature (4, 17), but 90 min after the loss of blood flow, transmission is decreased or absent in the infarct zone and in noninfarcted myocardium apical to the occlusion (4, 17, 18). These changes include the loss of nerve-stimulated effective refractory period shortening (4, 17) and denervation supersensitivity apical to the infarction (18). Decreased cardiac (4,16,22) and increased interstitial (1, 19) and plasma (22, 24) norepinephrine (NE) are also observed acutely after infarction due primarily to efflux of NE through the NE transporter (NET) (33).Loss of noradrenergic function in the infarct zone and in peri-infarct myocardium is retained for weeks or months after infarction. This is revealed by decreased accumulation of metaiodobenzylguanidine (9, 10, 14, 23) and NE (22), the absence of effective refractory period shortening on nerve stimulation (4), and the loss of catecholamine-containing nerve fibers in the left ventricle (LV) apical to the infarction (4). The loss of noradrenergic function, coupled with the absence of catecholamine-containing nerve fibers, is thought to be due to denervation of the infarct and peri-infarct z...

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“…Normal atria exhibit a heterogeneous distribution of vagal and sympathetic innervation. 18,21,27 An increased dispersion of atrial refractoriness has been observed in animal models of AF 2,6,7,28 and humans with paroxysmal AF. 9 Increased regional dispersion of AFCL appears to be an important independent determinant of electrophysiological remodeling and is observed even after shortening of atrial refractoriness caused by rapid pacing has stabilized.…”

Section: Role Of Sympathetic Innervation In Electrical Remodeling and Afmentioning

confidence: 99%

Atrial Fibrillation Produced by Prolonged Rapid Atrial Pacing Is Associated With Heterogeneous Changes in Atrial Sympathetic Innervation

et al. 2000

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Background-Structural and electrophysiological changes of the atria occur with prolonged rapid rates; however, the effects of sustained atrial fibrillation (AF) on autonomic innervation of the atria are unknown. We hypothesized that electrophysiological remodeling from rapid atrial rates is accompanied by altered atrial autonomic innervation. Methods and Results-Six dogs (paced group) underwent atrial pacing at 600 bpm; 9 dogs (control animals) were not paced. All paced dogs developed sustained AF by week 4 of pacing. All 15 animals underwent positron emission tomography imaging of the atria with [C-11] hydroxyephedrine (HED) to label sympathetic nerve terminals. HED retention in the atria was significantly greater in paced dogs compared with control animals (Pϭ0.03). Tissue samples from the atrial appendages had a greater concentration of norepinephrine in paced animals than in control animals (Pϭ0.01). The coefficient of variation of HED retention was also greater in paced animals (Pϭ0.05) and was greater in the right atrium than in the left atrium (Pϭ0.004). Epicardial activation maps of AF were obtained in the paced animals at baseline and with autonomic manipulation. Mean AF cycle length was longer in the right atrium (109.2Ϯ5 ms) than in the left atrium (85.8Ϯ5.5 ms) at baseline (Pϭ0.005). AF cycle length did not vary significantly from baseline (97.6Ϯ13.4 ms) with stellate stimulation (100.5Ϯ6 ms) but lengthened with propranolol (107.5Ϯ6.1 ms, Pϭ0.03). Conclusions-Rapid rates of AF produce a heterogeneous increase in atrial sympathetic innervation. These changes parallel disparate effects of rapid pacing-induced AF on atrial electrophysiology.

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Patterns of Sympathetic Nerve Projections onto the Canine Heart

Cited by 111 publications

References 6 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.

Infarction alters both the distribution and noradrenergic properties of cardiac sympathetic neurons

Atrial Fibrillation Produced by Prolonged Rapid Atrial Pacing Is Associated With Heterogeneous Changes in Atrial Sympathetic Innervation

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