Functional anatomy of canine cardiac nerves

Armour, J. Andrew; Randall, Walter C.

doi:10.1159/000144411

Cited by 67 publications

(19 citation statements)

References 6 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…When the right (stellate) CN in rats was stimulated, a chronotropic rather than inotropic effect was remarkably elicited, while stimulation of the left stellate CN or the thoracic CNs yielded only a marked inotropic action. Such differential effects of the electrical stimulation of the CNs of the right and left sides are much the same as those reported in dogs (LEVY et al, 1966;RANDALL et al, 1957RANDALL et al, , 1963 and may depend on different numbers of fiber populations innervating the pacemaker region and myocardium (ARMouR and RANDALL, 1975;RANDALL et' al., 1972).…”

Section: Discussionsupporting

confidence: 72%

Cardiac Sympathetic Nerves in Rats: Anatomical and Functional Features

Yasunaga

Nosaka

1979

Jpn.J.Physiol

View full text Add to dashboard Cite

1. Anatomical pathways and natures of reflex as well as spontaneous activities of cardiac sympathetic nerves (CNs) were investigated in rats. 2. Anatomically, the stellate CNs on both sides provide a major sympathetic supply to the rat heart with additional contribution of the thoracic CNs on the left side. 3. Functions of these CNs were studied in chloralose-urethane anesthetized and artificially ventilated rats. Electrical stimulation of these CNs produced an increase in heart rate and a rise in blood pressure. The increase in heart rate was more potent on the right-side stimulation, while the rise in blood pressure was greater on the left-side stimulation. 4. Stimulation of the aortic depressor nerve (ADN) inhibited spontaneous discharges of the CN for a longer period as compared with those of the cervical postganglionic sympathetic nerve (CSN). On the other hand, stimulation of the sural nerve produced a longer lasting reflex increase in discharges of the CN as compared with that of the CSN. These findings suggest that cardioregulatory sympathetic outflow is more affected by visceral and somatosensory input than is the other sympathetic outflows. 5. Spontaneous discharges of both nerves showed a rhythmicity associated with heart beats. Although the magnitude of this rhythmicity was not clearly different between these two nerves, the time from bottom to peak firing level of the phasic discharges of the CN was significantly longer than that of the CSN. This finding is consistent with the longer lasting effect of the ADN stimulation on the CN discharges.Since the cardiac nerve (CN) innervates the heart, including the conduction systems, myocardium and coronary arteries, its function can be regarded as purely circulatory and may differ from functions by the other sympathetic nerves. This assumption stems from the view that the activities of different sympathetic nerves show a non-uniform pattern NINOMIYA et al., 1970NINOMIYA et al., , 1971

show abstract

Section: Discussionsupporting

confidence: 72%

Cardiac Sympathetic Nerves in Rats: Anatomical and Functional Features

Yasunaga

Nosaka

1979

Jpn.J.Physiol

View full text Add to dashboard Cite

show abstract

“…By contrast, alpha-receptor or muscarinic cholinergic-mediated presynaptic inhibition of neuronal noradrenaline release could be ruled out in these studies, as was postsynaptic beta-receptor desensitization (4). A concomitant positive chronotropic effect was less pronounced during L-SNS, which is in line with previous observations in open-chest dogs (5,6). The comparable effects of R-SNS or L-SNS on ventricular inotropy and atrial refractoriness may be explained by a concomitant activation of afferent cardiac fibers (7).…”

Section: Discussionsupporting

confidence: 92%

Selective Increase of Cardiac Neuronal Sympathetic Tone

Zarse

Plisienė

Mischke

et al. 2005

Journal of the American College of Cardiology

View full text Add to dashboard Cite

show abstract

“…These findings concur with previous studies showing spontaneous sympathetic activation after low level vagal stimulation (Ardell et al, 2015; Kember et al, 2014; Onkka et al, 2013). Although the vagus nerve is historically considered the main component of the parasympathetic nervous system, morphological studies demonstrated that this nerve is composed, at the cervical level, by a small population of catecholaminergic fibers (Armour and Randall, 1975, Onkka et al, 2013 Verlinden et al, 2015). Furthermore, different electrical intensities of vagal stimulation can generate opposite effects depending on the “vagal-sympathetic balance”.…”

Section: Discussionmentioning

confidence: 99%

Modulation of experimental arthritis by vagal sensory and central brain stimulation

Bassi

Dias

Franchin

et al. 2017

Brain, Behavior, and Immunity

View full text Add to dashboard Cite

Articular inflammation is a major clinical burden in multiple inflammatory diseases, especially in rheumatoid arthritis. Biological anti-rheumatic drug therapies are expensive and increase the risk of systemic immunosuppression, infections, and malignancies. Here, we report that vagus nerve stimulation controls arthritic joint inflammation by inducing local regulation of innate immune response. Most of the previous studies of neuromodulation focused on vagal regulation of inflammation via the efferent peripheral pathway toward the viscera. Here, we report that vagal stimulation modulates arthritic joint inflammation through a novel "afferent" pathway mediated by the locus coeruleus (LC) of the central nervous system. Afferent vagal stimulation activates two sympatho-excitatory brain areas: the paraventricular hypothalamic nucleus (PVN) and the LC. The integrity of the LC, but not that of the PVN, is critical for vagal control of arthritic joint inflammation. Afferent vagal stimulation suppresses articular inflammation in the ipsilateral, but not in the contralateral knee to the hemispheric LC lesion. Central stimulation is followed by subsequent activation of joint sympathetic nerve terminals inducing articular norepinephrine release. Selective adrenergic beta-blockers prevent the effects of articular norepinephrine and thereby abrogate vagal control of arthritic joint inflammation. These results reveals a novel neuro-immune brain map with afferent vagal signals controlling side-specific articular inflammation through specific inflammatory-processing brain centers and joint sympathetic innervations.

show abstract

Functional anatomy of canine cardiac nerves

Cited by 67 publications

References 6 publications

Cardiac Sympathetic Nerves in Rats: Anatomical and Functional Features

Cardiac Sympathetic Nerves in Rats: Anatomical and Functional Features

Selective Increase of Cardiac Neuronal Sympathetic Tone

Modulation of experimental arthritis by vagal sensory and central brain stimulation

Contact Info

Product

Resources

About