Cardiac arrhythmias of sympathetic origin in the dog

1977 ◽  
Vol 233 (5) ◽  
pp. H535-H540
Author(s):  
L. S. D'Agrosa

The effects of ventrolateral and ventromedial cardiac nerve (left sympathetics) stimulation on cardiac force, on rate, and on arrhythmogenic responses were characterized and quantitated. The stimulation of left sympathetic nerves produced augmentation in cardiac contraction in 45% of the experiments, an augmentation of both a cardiac rate and force in 47%, and in cardioacceleration alone in 8%. Two characteristic patterns of arrhythmogenic responses were elicited from stimulations of 100 sympathetic nerves. The two types of neurally induced arrhythmias were atrioventricular junctional or ventricular in origin. The onset and duration of the arrhythmias were quantitated. Both types of neurally induced arrhythmias were prevented either by blocking the beta receptors with propranolol or by preventing the neural release of norepinephrine with bretylium tosylate. The neurally induced arrhythmias were probably the result of enhanced automaticity in the atrioventricular junction area and in the ventricles produced by stimulating the sympathetic nerve fibers. This report thus implicates the ventromedial cardiac nerve in the genesis of cardiac arrhythmias.

1981 ◽  
Vol 240 (4) ◽  
pp. H590-H596
Author(s):  
F. A. Kralios ◽  
C. K. Millar

The functional distribution of the cardiac sympathetic nerves to the atria and their arrhythmiogenic effects were determined in 16 open-chest pentobarbital-anesthetized dogs. Shortening of refractory periods at four right and two left atrial sites during stimulation of the nerves was taken as a criterion of their distribution. Stimulation of right stellate ganglion, craniovagal, and right stellate cardiac nerves produced localized shortening on the right atrium, particularly at the sinus node area, and invariably induced sinus tachycardia. The recurrent cardiac nerve produced little shortening at all sites and less arrhythmiogenic effect. The left stellate ganglion and ventrolateral cardiac nerve affected only left atrial sites and induced atrioventricular junctional rhythm. The ventromedial cardiac nerve affected all sites and had no consistent arrhythmiogenic effect. The innominate nerve had no substantial effect. We concluded that the functional distribution of the cardiac sympathetic nerves is localized, and that rate, rhythm, and refractory period changes induced by stimulation of these nerves are characteristic of the area of distribution.


2003 ◽  
Vol 145 (1-2) ◽  
pp. 77-85 ◽  
Author(s):  
Martin G. Kees ◽  
Georg Pongratz ◽  
Frieder Kees ◽  
Jürgen Schölmerich ◽  
Rainer H. Straub

2004 ◽  
Vol 286 (6) ◽  
pp. H2229-H2236 ◽  
Author(s):  
Wei Li ◽  
David Knowlton ◽  
Donna M. Van Winkle ◽  
Beth A. Habecker

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 [3H]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.


1995 ◽  
Vol 20 (5) ◽  
pp. 718-724 ◽  
Author(s):  
Paul Wigoda ◽  
David T. Netscher ◽  
John Thornby ◽  
Bianca Yip ◽  
Norman Rappaport

1979 ◽  
Vol 236 (4) ◽  
pp. H549-H553 ◽  
Author(s):  
M. L. Marcus ◽  
D. D. Heistad

Although cerebral blood vessels are densely innervated by sympathetic nerve fibers, the functional significance of the nerves is controversial. Because previous studies have been primarily performed in anesthetized animals, it is possible that failure to observe prominent neural control of the cerebral circulation was secondary to anesthetic-induced depression of the sympathetic nervous system. Therefore, we studied sympathetic control of the cerebral circulation in 11 awake chronically instrumented dogs. Total and regional cerebral blood flow was measured with 15-micrometer microspheres at control blood pressure and during three levels of progressive hemorrhagic hypotension. Sympathetic nerves had only a small effect (11% decrease; P less than 0.05) on flow to the cerebrum during moderate hypotension (mean arterial pressure 49 +/- 2 mmHg). Also, during severe hypotension, there was a bilateral redistribution of brain blood flow that tended to preserve flow to the medulla. Although these studies suggest that sympathetic nerves have a definite constrictor effect on cerebral vessels, the data support the concept that the functional importance of sympathetic nerves to cerebral vessels is limited.


Cephalalgia ◽  
1994 ◽  
Vol 14 (5) ◽  
pp. 320-327 ◽  
Author(s):  
L Edvinsson ◽  
PJ Goadsby

The cerebral circulation is invested by a rich network of neuropeptide Y (NPY) and noradrenaline containing sympathetic nerve fibers in arteries, arterioles and veins. However, the nerve supply of vasoactive intestinal peptide (VIP), substance P (SP) and calcitonin gene-related peptide (CGRP) containing fibers is sparse. While noradrenaline and NPY cause vasoconstriction, VIP, SP and CGRP are potent vasodilators. Stimulation of the trigeminal ganglion in cat and man elicits release of SP and CGRP. Subjects with spontaneous attacks of migraine show release of CGRP in parallel with headache. Cluster headache patients have release of CGRP and VIP during bouts. Treatment with sumatriptan aborts headache in migraine and cluster headache as well as the concomitant peptide release.


1976 ◽  
Vol 230 (4) ◽  
pp. 1003-1007 ◽  
Author(s):  
Y Uchida

The role of afferent cardiac sympathetic nerve fibers in the regulation of respiration has been examined. Application of potassium chloride or lactic acid solutions to the left ventricular surface of anesthetized vagotomized dogs resulted in a decrease in the manimum firing rate and shortening in period duration of firing of phrenic nerves. Also, application of the agents caused a decrease in amplitude and an increase in rate of respiratory thoracic movements. The same changes in phrenic nerve activity and respiratory movements were produced by coronary artery occlusion and centrifugal electrical stimulation of the left inferior cardiac nerves. The results indicate tachypnea that can be produced by excitation of afferent cardiac sympathetic nerve fibers.


1997 ◽  
Vol 36 (04/05) ◽  
pp. 290-293
Author(s):  
L. Glass ◽  
T. Nomura

Abstract:Excitable media, such as nerve, heart and the Belousov-Zhabo- tinsky reaction, exhibit a large excursion from equilibrium in response to a small but finite perturbation. Assuming a one-dimensional ring geometry of sufficient length, excitable media support a periodic wave of circulation. As in the periodic stimulation of oscillations in ordinary differential equations, the effects of periodic stimuli of the periodically circulating wave can be described by a one-dimensional Poincaré map. Depending on the period and intensity of the stimulus as well as its initial phase, either entrainment or termination of the original circulating wave is observed. These phenomena are directly related to clinical observations concerning periodic stimulation of a class of cardiac arrhythmias caused by reentrant wave propagation in the human heart.


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