Thoracic Vagus Research Articles

Distribution of calcitonin gene-related peptide-like immunoreactivity in the nucleus ambiguus of the cat.

The distribution of calcitonin gene-related peptide (CGRP) in the cat nucleus ambiguus was examined by means of a combination of horseradish peroxidase (HRP) tracing and immunohistochemical techniques. Vagal motoneurones in the nucleus ambiguus were identified by applying HRP to either the thoracic vagus or the superior laryngeal nerve or the cervical vagus. Motoneurones in the nucleus ambiguus labelled with HRP from the thoracic vagus did not contain CGRP-like immunoreactivity although CGRP-like immunoreactive cells were present in this nucleus on the same sections. In contrast, a large proportion of the motoneurones labelled from the superior laryngeal nerve and a smaller proportion of cells labelled from the cervical vagus did contain CGRP-like immunoreactivity. It is concluded that CGRP-like immunoreactivity is absent from vagal preganglionic motoneurones projecting to structures in the thorax and abdomen but is present in vagal motoneurones projecting to striated muscle of the larynx and pharynx.

Effect of sino-aortic denervation in comparison to cardiopulmonary deafferentiation on long-term blood pressure in conscious dogs.

The isolated and combined influence of cardiopulmonary and sinoaortic denervation on long-term blood pressure (MAP), heart rate (HR), plasma renin activity (PRA) and plasma volume (PV) was studied in 11 conscious, chronically instrumented foxhounds receiving a normal sodium diet. MAP, HR, PV and PRA remained unchanged in the 5 dogs after bilateral thoracic vagal stripping, which eliminates the cardiopulmonary afferents. After sino-aortic denervation in another 5 dogs there was equally little change when compared to the control group. Only total baroreceptor and cardiopulmonary denervation (7 dogs) revealed significantly higher levels of MAP (119.6 +/- 4.6 vs. 100.4 +/- 1.5, P less than 0.01), HR (118.2 +/- 3.7; vs. 84.1 +/- 3.5; P less than 0.0001), and PRA (3.6 +/- 0.9 vs. 0.9 +/- 0.2; P less than 0.05). In conclusion, the function of either arterial baroreceptors or cardiopulmonary receptors is sufficient for normal circulatory control. When both groups of receptor afferents are interrupted, MAP, HR, and PRA rise to significantly higher levels. Thus, both systems interact in a sense of a non-additive attenuation on "cardiovascular centres". This may clarify previous disputes concerning neurogenic hypertension, and supplies information for the role of the renin-angiotensin system in blood pressure control.

Desheathing the nodose ganglion is not a reliable method of de-efferentation in the ferret

The present study reports the results of physiological and anatomical experiments in which the purpose was to determine whether desheathing the nodose ganglion is a reliable method of vagal de-efferentation in the ferret. In physiological studies, the effects of electrically stimulating the treated and untreated vagal nerves on cardiovascular and intestinal responses were examined and compared with previously obtained data after left supranodose vagotomy. The anatomical studies illustrated the effects of desheating the left nodose ganglion on the transport of horseradish peroxidase (HRP) within a thoracic vagal communicating branch. These data were compared to data from control animals and animals that had undergone left supranodose vagotomy. The results demonstrated that severing the fascicles overlying the left nodose ganglion and allowing the nerve fibers to degenerate, caused no reduction in labeled efferent cell bodies in the left dorsal motor nucleus of the vagus as compared to controls. However, after left supranodose vagotomy there were no efferent cell bodies labeled in the left dorsal motor nucleus of the vagus. Following degeneration of the fascicles, electrical stimulation of the peripheral cut end of this nerve did not abolish the efferent responses in 7 out of 9 animals studied, whereas supranodose vagotomy abolished the responses in all animals. These findings demonstrate that desheathing the nodose ganglion and thereby removing the nerve bundles overlying the nodose ganglion is not a guaranteed method of destroying the efferent fibers in the vagus nerve of the ferret. Supranodose vagotomy, therefore, is a more reliable method of de-efferentation in this species.

The influence of cardiopulmonary receptors on long-term blood pressure control and plasma renin activity in conscious dogs.

The isolated and combined influence of cardiopulmonary and arterial baroreceptor denervation on long-term blood pressure (MAP), heart rate (HR), plasma volume (PV) and plasma renin activity (PRA) was studied in 10 conscious, chronically instrumented foxhounds receiving a normal sodium diet. Cardiopulmonary denervation was achieved by surgically stripping both thoracic vagi. Near complete arterial baroreceptor denervation, leaving most cardiopulmonary fibres intact, was made by left vagal deafferentiation which has been shown to eliminate most aortic baroreceptor afferents, and a carotid sinus denervation. Five groups were studied: (I) control (n = 9), (II) cardiopulmonary denervation (n = 5), (III) aortic baroreceptor denervation (n = 5), (IV) arterial baroreceptor denervation (n = 4) and (V) total denervation (n = 6). No changes in PV were observed. Only group V revealed significantly higher levels of MAP (119.5 +/- 5.4 vs. 100.1 +/- 1.6 mmHg; P less than 0.05), HR (118.1 +/- 4.4 vs. 87.8 +/- 3.7 beats min-1; P less than 0.001) and PRA (3.0 +/- 0.8 vs. 0.9 +/- 0.2 ng AI m-1 h-1; P less than 0.05). It is suggested that the isolated function of either cardiopulmonary or arterial baroreceptors is sufficient to maintain these variables at a normal level. Contrary to the results of other reports the cardiopulmonary receptors do not seem to regulate MAP at a level about which the arterial baroreceptors operate. When both groups of afferents were interrupted MAP, HR and PRA rose to significantly higher levels, implying that cardiopulmonary and arterial baroreceptor afferents interact in a sense of a non-additive attenuation.

Effects of vagal deafferentation on oesophageal motility and transit in the sheep.

Effects of vagal deafferentation on oesophageal motility and transit were studied in conscious sheep by recording the electromyographic activity of different parts of oesophagus during swallowing of saliva, or balloons inflated with 20 ml of air. Surgical isolation and subsequent sectioning of the nodose ganglion, leaving the bundles of motor fibres intact, can be performed in sheep. Division of both ganglia led to immediate death of sheep. However, vagal deafferentation of the thoracic oesophagus could be achieved by sectioning the thoracic vagus nerve in association with sectioning the contralateral nodose ganglion. The sectioning of one vagus nerve did not affect primary oesophageal peristalsis during swallowing of saliva or of a bolus. Balloons inflated in the pharyngeal cavity and left free to move caudally, failed to pass into the stomach within the normal time of 2-2.3 s in only 4-16% of the tests. In these cases, they were always stopped in the thoracic oesophagus. Following total deafferentation of the thoracic oesophagus, balloons were prevented from being propelled into the stomach in each test. They were stopped for several minutes at the beginning of the deafferented part of the oesophagus. Electromyographic activity recorded from the deafferented part was reduced during swallowing of balloons or saliva. Deafferentation was confirmed by the failure of the presumed deafferented segment of oesophagus to respond to distension. These experiments provide direct evidence that the vagus carries information from the oesophagus which influences the central pattern generator during swallowing of a bolus or saliva. In sheep, this feed-back is essential for the effective swallowing of a bolus although not for saliva.

Effect and mechanism of vagal nerve stimulation on somatostatin secretion in dogs.

To investigate the effect of vagal nerve stimulation on the release of pancreatic somatostatin, we electrically stimulated (10 Hz, 5 ms, 13.5 mA, and 10 min) the thoracic vagi just below the heart in halothane anesthetized dogs (n = 15). The stimulation increased the pancreatic output of somatostatinlike immunoreactivity (SLI) (delta = +248 +/- 81 fmol/min, P less than 0.005; base-line levels = 455 +/- 150 fmol/min). min). Arterial plasma SLI levels increased as well (delta = +16 +/- 3 fmol/ml, P less than 0.001; base-line levels = 65 +/- 3 fmol/ml), reflecting stimulation of extrapancreatic SLI secretion. Significant vagal activation was verified by a fivefold increase of pancreatic output of pancreatic polypeptide (PP) (delta = +31.4 +/- 5.9 ng/min, P less than 0.001; base-line levels = 7.8 +/- 0.9 ng/min). Atropine pretreatment (n = 6) inhibited partially both the PP response (delta = +7.9 +/- 3.8 ng/min after atropine) and the pancreatic SLI response (delta = +92 +/- 29 fmol/min) to vagal nerve stimulation. However, atropine pretreatment did not modify the arterial SLI response (delta = +20 +/- 7 fmol/ml). Hexamethonium pretreatment (n = 9) completely abolished all three responses. We conclude that 1) electrical stimulation of the vagus stimulates pancreatic SLI, extrapancreatic SLI, and PP release in vivo in the dog; 2) both muscarinic and nonmuscarinic mechanisms mediate the PP and pancreatic SLI responses; 3) a nonmuscarinic mechanism mediates the extrapancreatic SLI response; and 4) all three responses are mediated via ganglionic nicotinic receptors.

The influence of cholinergic and adrenergic blockade on the portal release of substance P in the cat

The effect of efferent electrical stimulation of the divided thoracic vagus nerves on the release of substance P-like immunoreactivity (SPLI) into the portal vein was studied in anesthetized cats. Under basal conditions portal SPLI levels were fairly constant. During the first 5 min of vagal stimulation there was a significant increase of the portal plasma levels of SPLI. Since we have demonstrated that infracardiac vagal stimulation causes only minor changes in small intestinal bloodflow, a true vagal neurogenic release of SPLI seems likely. We have shown that SPLI is exclusively localized within feline gut neurons (not the enterochromaffin (EC) cells). Thus, SPLI released into the portal circulation probably represents overflow of transmitter into the circulation. Neither blockade of cholino- or adrenoceptors nor ganglionic blockade influenced the enhanced release of SPLI induced by vagal stimulation, suggesting activation of SP neurons via nonclassical receptors.

Differential responses accompanying sequential stimulation and ablation of vagal branches to dog heart.

Electrical excitation of small thoracic vagal branches elicited highly localized responses in the canine heart. Specific pathways to the sinoatrial nodal (SAN) regions were identified from negative chronotropic responses to stimulation (20 Hz, 5.0 ms, 3.0-5.0 V) of these branches. Pathways to the atrioventricular nodal (AVN) region were determined from changes in A-H interval (His bundle electrogram) and incidence of heart block as vagal branches were stimulated during concurrent atrial pacing. A few small branches influenced a single cardiac function (atrial rate, contractile force, or AV conduction). More commonly, activation of such branches elicited simultaneous chronotropic and dromotropic effects. However, many branches failed to elicit any detectable cardiac change. The major outflow from the left vagus to SAN and AVN regions is by way of cardiac branches from the recurrent laryngeal nerve at its reflection around the aorta. Activation of the left recurrent nerve reduced atrial rate by 43% and doubled A-H interval 84 to 167 ms. The right thoracic vagus or its branches induced A-H prolongation from 78 to 131 ms. H-V intervals remained constant at a mean of 35 ms. Outflows from the right thoracic vagus to SAN and/or AVN regions originated just below the middle cervical ganglion and at all levels down to the azygos vein.

T2-T5 spinothalamic neurons projecting to medial thalamus with viscerosomatic input.

Spinothalamic tract neurons projecting to medial thalamus (M-STT cells), ventral posterior lateral nucleus (VPL) of the thalamus (L-STT cells), or both thalamic regions (LM-STT cells) were studied in 19 monkeys anesthetized with alpha-chloralose. Twenty-seven M-STT cells were antidromically activated from nucleus centralis lateralis, nucleus centrum medianum, or the medial dorsal nucleus. Stimulation of VPL elicited antidromic responses from 22 cells and 13 cells were activated from both VPL and medial thalamus. Antidromic conduction velocities of M-STT cells were significantly slower than those of L-STT or LM-STT cells. M-STT cells were located in laminae I, IV, V, and VII with greater numbers found in the deepest laminae. L-STT cells were located mostly in lamina IV, whereas most LM-STT cells were found in lamina V. Twenty-four of 27 M-STT cells, all L-STT cells, and all LM-STT cells received input from both cardiopulmonary sympathetic and somatic afferent fibers. WDR cells were most common among the L-STT and LM-STT groups, whereas HT cells were the most common class in the M-STT cell group. Excitatory receptive fields of M-STT cells were large, and often bilateral. Receptive fields of L-STT cells were simple and never bilateral. Receptive fields of LM-STT cells could be similar to M-STT or L-STT cells. Thirty-three percent of the M-STT cells, 37% of the L-STT cells, and 62% of the LM-STT cells had inhibitory receptive fields. Inhibition was elicited most often by a noxious pinch of the hindlimbs. Sixteen of 23 (70%) M-STT cells received C-fiber cardiopulmonary sympathetic input in addition to A-delta-fiber input. The other 7 cells received only A-delta-fiber input. Only 45% of the L-STT cells and 38% of the LM-STT cells received both A-delta- and C-fiber inputs. The maximum number of spikes elicited by A-delta-input was related to segmental locations for L-STT cells with greatest responses in T2 and lesser responses in more caudal segments; however, no such trend was apparent for M-STT cells or for responses to C-fiber input for either group. Electrical stimulation of the left thoracic vagus nerve inhibited 7 of 18 M-STT cells, 10 of 16 L-STT cells, and 6 of 12 LM-STT cells. These results are the first description of visceral input to cells projecting to medial thalamus.(ABSTRACT TRUNCATED AT 400 WORDS)

The role of oesophageal and intestinal receptors in the control of gastric motility

The aim of this work was to characterize the discharge pattern of vagal efferent fibers supplying the stomach, and the modifications of this pattern induced by stimulation of oesophageal or intestinal receptors. The experiments were performed on dogs in which the central end of the left thoracic vagus had been sutured to the peripheral end of the left phrenic nerve. In such preparations, the activity of the motor units of the reinnervated left hemidiaphragm indicated the activity of vagal efferent fibers. After the left hemidiaphragm had been transformed into subcutaneous muscle, it was possible to study, using electromyography, in the conscious dog, the discharge of efferent vagal fibers which originally supplied the stomach. All the gastric vagal efferent fibers presented a spontaneous discharge with a very low frequency (0.1 Hz < f < 5 Hz). The firing of some fibers was increased each time the gastric motility was enhanced: these fibers were considered to be excitatory fibers. In contrast, other fibers exhibited an opposite discharge pattern and they were considered to be inhibitory fibers. Among all the gastric fibers whose activity was recorded in this study, some of them presented a modification of discharge during the receptive relaxation of the proximal stomach produced by an oesophageal distension. The discharge of excitatory fibers was suppressed while that of the inhibitory fibers was markedly increased. Taking into account these modifications of discharge, parallel to the relaxation of the proximal stomach, it was assumed that these fibers originally supplied the gastric fundus. Other fibers whose discharge remained unchanged during receptive relaxation were supposed to supply the distal stomach, i.e. the gastric antrum. During gastric emptying, when a small inflated baloon, propelled by gastric peristalsis entered the duodenum, the discharge frequency of all the excitatory fibers was decreased whereas that of the inhibitory fibers was enhanced. Similar variations of discharge were observed during the enterogastric inhibitory reflex, caused by an intraduodenal infusion of hydrochloric acid.

Coronary venous pressure and flow: effects of vagal stimulation, aortic occlusion, and vasodilators.

Coronary venous pressure and coronary sinus flow in the canine heart were compared with intramyocardial, intraventricular, aortic, and coronary artery pressures. Stimulation of the thoracic vagus augmented coronary venous pressure, mean venous flow per systole, and coronary venous systolic resistance, but decreased the mean venous flow. Partial occlusion of the aorta augmented coronary venous pressure and coronary venous flow, while systolic coronary venous resistance remained unchanged. Adenosine increased peripheral and central coronary venous pressure and venous flow; it reduced peripheral coronary artery pressure. Adenosine augmented flow per systole and reduced venous resistance more than the other interventions. Dipyridamole decreased left ventricular, aortic, and central coronary artery systolic pressures and systolic venous resistance. It increased the venous flow, mean flow per systole, and coronary venous pressure, even though intramyocardial pressure remained unchanged. Nitroglycerine elevated coronary venous pressure and flow, as well as venous flow per systole, even though it decreased left ventricular, aortic, and central coronary artery pressures. Nitroglycerine significantly decreased coronary venous resistance. It is concluded that coronary venous resistance may be an important resistive component to consider when the total coronary circulation is studied.

Greater splanchnic excitation of primate T1-T5 spinothalamic neurons.

Effects of electrical stimulation of the left greater splanchnic nerve (SPL) on T1-T5 spinothalamic (STT) neurons were determined. Eighty-five STT neurons were studied in 36 anesthetized monkeys (Macaca fascicularis). All neurons were excited by manipulation of their somatic receptive fields and by electrical stimulation of cardiopulmonary (CP) sympathetic afferent fibers. SPL stimulation excited 63 (74%) STT neurons. There was an increasing percentage of cells with SPL input at more caudal segments and in deeper laminae. Both SPL and CP sympathetic stimulation elicited early or both early and late responses. Latencies to cell activation were usually shorter for CP sympathetic stimulation than for SPL stimulation (5.4 +/- 0.8 versus 11.3 +/- 2.0 ms for early responses and 44.2 +/- 4.2 versus 111.0 +/- 6.6 ms for late responses). The maximum number of spikes per SPL or CP sympathetic stimulus was determined. In the T2 and T3 segments, early responses to CP sympathetic stimulation were significantly greater. However, at more caudal segments, responses to CP sympathetic input decreased while responses to SPL input increased until at T4 there was no difference in the two responses. In T5, responses to SPL input were greater. No differences in the magnitudes of late responses were observed in any of the segments. The response of six cells to SPL stimulation was inhibited by a train of conditioning stimuli applied to the left thoracic vagus nerve. Maximum inhibition occurred at a CT interval of 50 ms and test responses were significantly reduced at CT intervals as great as 200 ms. Bilateral vagotomy eliminated the inhibitory effect. Cutting the left sympathetic chain between the T5 and T6 rami communicantes eliminated 27% of the response to SPL stimulation. More caudal cuts reduced the response further until 71% of the response was abolished by a cut between T8 and T9. Lesions in the dorsolateral column of the spinal cord had little effect on the responses, while lesions of the lateral and ventrolateral columns reduced or abolished the responses. We conclude that SPL stimulation excites T1-T5 STT neurons by way of extraspinal and intraspinal pathways. SPL information is integrated with information from a variety of other visceral and somatic sources. SPL input to cells with somatic fields in the chest region may explain the clinical phenomenon of chest pain associated with abdominal disorders.

Vagal afferent inhibition of spinothalamic cell responses to sympathetic afferents and bradykinin in the monkey.

Effects of stimulating the left thoracic vagus nerve on the responses of spinothalamic neurons to electrical stimulation of cardiopulmonary sympathetic afferent fibers and to intracardiac injections of bradykinin were determined. Experiments were performed on 39 monkeys (Macaca fascicularis) tranquilized with ketamine and anesthetized with alpha-chloralose. The 30 spinothalamic cells studied had the following characteristics. They were excited by manipulation of their somatic receptive fields, were excited by electrical stimulation of cardiopulmonary sympathetic afferent fibers, and exhibited viscerosomatic convergence. Responses of 15 of 19 cells to sympathetic afferent test stimuli were inhibited by conditioning stimuli applied to left thoracic vagus nerve. A conditioning-test interval of 40-50 msec resulted in maximal inhibition of responses to both A delta and C fiber sympathetic afferents. A long time course of inhibition was present to at least a conditioning-test interval of 200 msec. Left thoracic vagus nerve stimulation inhibited 14 of 14 cells responding to intracardiac injection of bradykinin. Entrainment of activity of five cells to the cardiac cycle occurred in response to bradykinin. In each case, left thoracic vagus nerve stimulation, in addition to reducing frequency of cell discharge, disrupted the cardiac related pattern of cell activity. Bilateral cervical vagotomy abolished all inhibitory effects of left thoracic vagus nerve stimulation. These results demonstrate that vagal afferents may participate in processing of information related to cardiac pain.

Reversible truncal vagotomy in conscious dogs

Prior attempts at in vivo reversible vagal denervation of the gastrointestinal tract have been limited to cervical cooling techniques that also denervate both sympathetic and vagal pulmonary and cardiac branches. Denervation of vagal efferent fibers at this level has produced results that are inconsistent with those obtained after surgical truncal vagotomy. We have, therefore, developed a technique to provide reversible vagal denervation below the pulmonary and cardiac branches for the study of gastric motility. Five dogs, previously equipped with gastric strain gages and electrodes, underwent implantation of a tubular cooling jacket around a distal thoracic vagal trunk with contralateral vagotomy (4 dogs), or around both vagal trunks (1 dog). The jacket was made of stainless steel tubing in a “J” design. Its inside channel was lined with a sterling silver sheet, and a thermistor was attached to record temperature change. Silicone tubing coursed externally to a pump and flask to which 95% ethanol at −70 °C was circulated at variable speeds. Thoracic vagal cooling, extending up to 5 h, reversibly blocked gastric contractions induced by insulin hypoglycemia. Contractile waves were terminated at device temperatures of 2 °–6 °C but promptly returned with warming. Dogs were tranquil during denervation, and enclosed nerves remained functional for >40 days.

Reinnervation of striated muscle by peripheral vagal fibres cut above or below the nodose ganglion in the cat and rabbit.

In cats and rabbits, the peripheral stump of the vagus nerve cut above the nodose ganglion (supranodose anastomoses: s.n.) or below this ganglion (infranodose anastomoses: i.n.) was either sutured with epineurial sutures to the peripheral stump of the branch of the spinal accessory motor nerve innervating the sterno-cleido-mastoid (s.c.m.) muscle, or directly implanted in this muscle after resection of its motor nerve. After about six months, reinnervation of this muscle by vagal fibres was studied. By electromyographic recording during electrical stimulation of the cervical vagus nerve, it was shown that the vagal reinnervation of the s.c.m. muscle was established in 65% of the cats studied (57% s.n., 69% i.n.) and 33% of rabbits (37% s.n. and 31% i.n.). The average number of distinct potentials recorded in the reinnervated muscle, following vagal stimulation, was twenty-two in s.n. cats, thirteen in i.n. cats, eleven in s.n. rabbits and twelve in i.n. rabbits. Recorded potentials were monophasic (8%), biphasic (22.5%), triphasic (11.5%) or polyphasic (58%). These potentials were abolished by curare and alpha-bungarotoxin. The use of retrograde axonal transport of horseradish peroxidase showed labelled cells in the nodose ganglion, the cervical vagus and cranial thoracic vagus, and in the stellate ganglia. It is concluded that cholinergic vagal afferents reinnervated the s.c.m. muscle. Involvement of the sympathetic system is discussed.

Synaptic transmission in the decentralized middle cervical ganglion of the dog

The middle cervical ganglion (MCG) was decentralized in 30 dogs by cutting the thoracic vagus and rami on one side. Two or more cardiopulmonary nerves were then dissected free and placed on bipolar stimulating and recording electrodes in mineral-oil baths. Stimulation of one cardiopulmonary nerve generated a compound action potential (CAP) in one or two others. The CAP was altered by changing the frequency of stimulation and by stimulating preganglionic fibers in the rami. These alterations displayed latency changes and temporal summation or inhibition. The ansae were sectioned to neurally isolate the MCG from the stellate ganglion. A CAP generated after blockade by hexamethonium, atropine, propranolol and phentolamine was abolished transiently by chymotrypsin, and for longer periods by manganese, injected locally into the MCG. These results suggest that a CAP that is generated by stimulating one cardiopulmonary nerve in a decentralized MCG and recorded from another may result from synaptic activity in the MCG and that complex neuronal interactions occur within the MCG.

Physiological studies of canine sympathetic ganglia and cardiac nerves

Anatomical studies have indicated that the middle cervical ganglion is the primary locus of sympathetic postganglionic neurons which have axons projecting in canine cardiac nerves. Small regions of thoracic sympathetic ganglia were stimulated electrically with bipolar electrodes and the generated compound action potentials were recorded from ipsilateral cardiac nerves. Several procedures were used to distinguish the effects of stimulating preganglionic axons, ganglionic sites and postganglionic axons. Following hexamethonium it was found that only low frequency stimulation (e.g. 1 Hz) of ganglionic sites resulted in the generation of compound action potentials in cardiac nerves. These ganglionic sites were located throughout the middle cervical ganglion, but only in the cranial medial pole of the stellate ganglion. Stimulation of a single locus in a stellate or middle cervical ganglion generated compound action potentials in all major ipsilateral sympathetic cardiac nerves. A ganglion was also identified at the junction of the thoracic vagus and the cranial vagal nerve which may be as important as the right stellate ganglion in cardiac regulation. These results demonstrate that there are discrete loci in thoracic ganglia which contain neurons projecting in several ipsilateral cardiac nerves. Low frequency stimulation of these loci was found to be optimal for generation of compound action potentials.

Effect of cervical and thoracic vagal stimulation on luminal serotonin release and regional blood flow in cats

In acute experiments on 14 cats, the transected vagus nerves were stimulated at two levels (10 V, 5 ms, 10 Hz, 10 mA, 15 min). Fifteen-centimeter proximal jejunal segments were perfused with saline (1.0 ml/min). Basal luminal immunoreactive serotonin secretion averaged 206 ± 67 ng/5 min. After stimulation of the vagus nerves, there was an immediate two- to threefold increase in the rate of secretion of immunoreactive serotonin into the lumen. There were no significant differences in the stimulated secretory rates that resulted from stimulation at the cervical or thoracic levels. Shortly after cessation of vagal stimulation, immunoreactive serotonin secretory rates returned to basal. Vagal nerve stimulation did not result in any change in peripheral or portal venous blood concentrations of serotonin. In 12 additional cats, the effects of stimulation of the vagus nerves at the cervical and thoracic levels on regional blood flow, as determined using the microsphere technique, were compared. Cervical vagal stimulation resulted in hypotension, bradycardia, decreased perfusion of the heart, kidney, and small and large bowels, but preservation of the perfusion of the fundus and antrum. In contrast, stimulation of the transected nerves in the chest stimulated gastric blood flow but did not alter either flow to other viscera or central hemodynamics.

Effects of individual cardiac nerve stimulation on atrioventricular conduction

This study investigated the effects of individual canine cardiac nerve stimulation on atrioventricular conductions as measured by His bundle electrograms. A-H and H-V intervals were measured before and during stimulation of each nerve in paced hearts (200 beats/min) and before and after blocking doses of either atropine or propranolol. Increases in A-H or H-V intervals were evidence of parasympathetic innervation; decreases in intervals were evidence of sympathetic innervation. Separation by autonomic composition produced 3 categories: sympathetic, parasympathetic, and mixed input to the atrioventricular junction. The sympathetic nerves were the left and right ansae subclavia, the ventrolateral cardiac nerve, and the right stellate cardiac nerve. The parasympathetic nerve was the right thoracic vagus, and the mixed nerves were the left thoracic vagus, and the innominate, ventromedial, craniovagal, caudovagal, and right recurrent cardiac nerves. The cardiac nerves eliciting a major response were the left and right ansae subclavia, the ventrolateral, right recurrent, craniovagal, and caudovagal cardiac nerves, and the left and right thoracic vagi. In theory, the nerves of the right side, because of their innervation of both sinoatrial and atrioventricular nodes, may be expected to elicit a balanced heart rate-atrioventricular conduction response when stimulated, thus matching atrial and ventricular rates. On the other hand, stimulation of the ventrolateral cardiac nerve regularly produces dysrhythmia, due to increased automaticity at the atrioventricular junction. Production of such arrhythmias indicates the possible implication of imbalanced autonomic activity in arrhythmogenesis. Three cardiac nerves produced little or no effect on atrioventricular conduction. These were the innominate, ventromedial, and right stellate cardiac nerves. Because of its limited distribution and marked sinus rate effects, the right stellate cardiac nerve can be considered almost a purely positive chronotropic nerve. Its possible role in heart rate-atrioventricular conduction mismatching has not been delineated but, because of its nearly exclusive action at the sinoatrial node, may be of considerable importance.

Nervous control of pancreatic endocrine secretion in pigs. V. Influence of the sympathetic nervous system on the pancreatic secretion of insulin and glucagon, and on the insulin and glucagon response to vagal stimulation.

Electrical stimulation of the splanchnic nerves in anesthetized pigs was found to stimulate markedly the pancreatic secretion of glucagon. The response pattern was glucose dependent, the glucagon responses at blood glucose concentrations below 4.5 mmol x l-1 being significantly greater than those noted during stimulation at higher concentrations. Insulin secretion was stimulated weakly and variably and only at higher glucose levels. The magnitude of the glucagon response was comparable to that obtained by electrical stimulation of the thoracic vagus nerves with the same frequency. The glucagon response to combined vagal and splanchnic stimulation was nearly identical to the sum of the responses to the two types of stimulation, whereas splanchnic stimulation abolished or reduced the increase in insulin secretion elicited by vagal stimulation. Combined alpha- and beta-adrenergic blockade markedly reduced the glucagon responses to splanchnic stimulation.