Longitudinal distribution of negative cord dorsum potentials following stimulation of afferent fibres in the left inferior cardiac nerve

1986 ◽  
Vol 17 (3) ◽  
pp. 185-197 ◽  
Author(s):  
Dariusz Nowicki ◽  
Pawel Szulczyk
1984 ◽  
Vol 247 (5) ◽  
pp. R761-R767 ◽  
Author(s):  
S. M. Barman ◽  
G. L. Gebber

This study tested the hypothesis that at least some brain stem and reflex control of sympathetic outflow is mediated over pathways containing spinal interneurons. The vicinity of the intermediolateral nucleus (IML) of the third thoracic spinal segment was searched for neurons with spontaneous activity correlated to that in the inferior cardiac post-ganglionic sympathetic nerve of 16 baroreceptor-denervated cats anesthetized with Dial-urethane. Section of the carotid sinus, aortic depressor, and vagus nerves prevented the coupling of sympathetic and nonsympathetic networks by pulse synchronous baroreceptor activity. Spike-triggered averaging revealed the existence of two types of spinal neurons with sympathetic nerve-related activity. Preganglionic sympathetic neurons (PSN; n = 33) were antidromically activated by electrical stimulation of their axons in the third thoracic white ramus. Four observations suggest that the second group of neurons with sympathetic nerve-related activity (n = 18) were spinal interneurons (SIN) in pathways that excite PSN. First, these neurons could not be antidromically activated by stimulation of the segmental white ramus. Second, the intervals between spontaneous unit spike occurrence and inferior cardiac nerve activity were similar for SIN and PSN. Third, SIN and PSN were activated with nearly identical onset latencies by electrical stimulation of medullary sympathoexcitatory sites. Fourth, SIN were excited by intensities of cardiac sympathetic afferent stimulation that also activated PSN and the inferior cardiac nerve. SIN and PSN were distinguished on the basis of their spontaneous firing patterns; i.e., interspike intervals of SIN were significantly shorter than those of PSN.(ABSTRACT TRUNCATED AT 250 WORDS)


1995 ◽  
Vol 268 (6) ◽  
pp. R1472-R1483 ◽  
Author(s):  
G. L. Gebber ◽  
S. Zhong ◽  
S. M. Barman

We used phase spectral analysis to study the relationships between the cardiac-related discharges of pairs of postganglionic sympathetic nerves in urethan-anesthetized or decerebrate cats. Phase angle when converted to a time interval should equal the difference in conduction times from the brain to the nerves (i.e., transportation lag) if their cardiac-related discharges have a common central source. Transportation lag was estimated as the difference in the onset latencies of activation of the nerves by electrical stimulation of the medulla or cervical spinal cord. The phase angle for the cardiac-related discharges of two nerves was not always equivalent in time to the transportation lag. For example, in some cases the cardiac-related discharges of the renal nerve were coincident with or led those of the inferior cardiac nerve. In contrast, the electrically evoked responses of the renal nerve lagged those of the inferior cardiac nerve by > or = 32 ms. These observations are consistent with a model of multiple and dynamically coupled brain stem generators of the cardiac-related rhythm, each controlling a different sympathetic nerve or exerting nonuniform influences on different portions of the spinal sympathetic outflow.


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.


1975 ◽  
Vol 229 (2) ◽  
pp. 286-290 ◽  
Author(s):  
M Pagani ◽  
PJ Schwartz ◽  
VS Bishop ◽  
A Malliani

In anesthetized vagotomized cats with the chest opened and artificially ventilated, aortic blood pressure (AP) and external diameter (AD; ultrasound technique) were measured in the proximal third of the descending thoracic aorta. Slow sinusoidal oscillations (0.2-0.3 Hz in aortic volume were produced by a piston pump connected to a femoral artery. Diastolic pressure-diameter relationship (PDR) curves were obtained during control conditions and during stimulation of either the cut central end of the left inferior cardiac nerve (ICN) or the decentralized thoracic sympathetic chain (SC). In six cats with both carotid arteries occluded ICN stimulation reflexly shifted the PDR curves to lower diameters for any given pressure (mean deltaAD 3.2% at control AP). A smaller response to ICN stimulation was obtained in five cats with one patent carotid artery (mean deltaAD 2.3% at control AP). Stimulation of sympathetic efferents to the aorta (SC) caused similar responses in five animals (mean deltaAD 3.4% at control AP). This reflex control of the thoracic aorta may be involved in cardioaortic coupling and may influence the sensitivity of aortic mechanoreceptors.


1977 ◽  
Vol 232 (6) ◽  
pp. H590-H595 ◽  
Author(s):  
D. R. Kostreva ◽  
E. J. Zuperku ◽  
J. F. Cusick ◽  
J. P. Kampine

The sympathetic efferent contribution of left ventral roots T2, T3, and T4 to some cardiac nerves was studied using evoked potentials in mongrel dogs anesthetized with sodium pentobarbital. Electrical stimulation of the ventral roots while recording evoked potentials from the sympathetic chain, anterior ansa subclavia, posterior ansa, ventrolateral cervical cardiac nerve, ventromedial cervical cardiac nerve, and the vagosympathetic trunk demonstrated that A-, B-, and C-type fibers exist in these efferent neural pathways. The range of conduction velocities observed was 0.7-104 m/s. T2 contributed the largest number of A-type fibers, and T2 and T3 contributed C-type fibers equally, while T4 had the least number of fibers coursing through the cardiac nerves.


1959 ◽  
Vol 197 (1) ◽  
pp. 217-222 ◽  
Author(s):  
Irvine H. Page ◽  
J. W. McCubbin

Tetraethylammonium, hexamethonium, chlorisondamine or mecamylamine suppressed the dog's carotid occlusion reflex well before appearance of maximum augmentation of responses to pressor drugs. The reflex usually returned to near control values despite continued administration of ganglioplegics, while augmented responsiveness persisted or became more marked. An antipseudocholinesterase or prostigmine restored the suppressed reflex without loss of augmented responsiveness. Electroneurographic measurements of efferent spontaneous activity in postganglionic renal nerves revealed synaptic pathways resistant to blockade: a small amount of activity persisted during tolerance to ganglioplegics and showed reflex changes. Similar measurements of spontaneous and evoked potentials in the inferior cardiac nerve showed no synaptic activity during tolerance. Augmentation of response to pressor drugs by ganglioplegics does not depend wholly upon loss of compensatory reflexes; peripheral sensitization is probably another mechanism concerned. Maintenance of arterial pressure and persistence of cardiovascular reflexes during tolerance to ganglioplegics appear to depend upon transmission of a relatively few impulses over pathways resistant to blockade and upon peripheral sensitization to the presumably smaller amounts of norepinephrine released from nerve endings.


1979 ◽  
Vol 236 (2) ◽  
pp. H286-H290
Author(s):  
R. S. Tuttle ◽  
M. McCleary

A number of studies in this and other laboratories using hemodynamic and pharmacologic evidence have suggested that occlusion of the mesenteric artery evokes a pressor reflex initiated by mesenteric baroreceptors. To provide additional evidence in support of this hypothesis, neurophysiological recordings were made of inferior cardiac nerve activity during mesenteric artery occlusion (MAO). The results indicate that MAO enhances inferior cardiac nerve activity in the cat, providing that the carotid sinus nerves have been cut. Cutting of the mesenteric nerves further facilitates cardiac nerve activity and abolishes the response to mesenteric artery occlusion. The evidence suggests that MAO evokes a reflex sympathetic discharge which is subject to override by the carotid sinus depressor reflex. The afferent limb of the reflex is characterized by a tonic depressor outflow from the mesenteric pressure receptors.


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