The hyperglycaemic response to stimulation of the hepatic sympathetic innervation in adrenalectomized cats and dogs

1. The extent to which the hyperglaemic and glycogenolytic responses to splanchnic nerve stimulation depend upon the integrity of the hepatic innervation has been investigated in adrenalectomized dogs and cats.2. In both species maximal stimulation of the hepatic nerves (20 c/s) produced changes in plasma glucose concentration comparable to those which have been found to occur in response to bilateral splanchnic nerve stimulation at the same frequency. Furthermore, the hyperglycaemic response to splanchnic nerve stimulation was very substantially reduced by section of the hepatic nerves, whereas the associated changes in haematocrit and mean aortic blood pressure were not significantly altered.3. Comparison of the changes in plasma glucose concentration in response to splanchnic or hepatic nerve stimulation at relatively low frequencies (1.0-2.0 c/s) showed that stimulation of either nerve produced closely similar responses in adrenalectomized animals of both species.4. In adrenalectomized dogs maximal stimulation of the hepatic nerves (20 c/s) for shorter periods (30 sec) caused a significant rise in plasma glucose concentration whereas total occlusion of the portal vein for the same period in the same animals produced no statistically significant hyperglycaemic effect.5. Maximal stimulation of the hepatic nerves (20 c/s) caused a rapid rise in plasma glucose concentration in hypoglycaemic adrenalectomized cats pretreated with a large dose of insulin (4 u./kg body wt.).6. It is concluded that the hyperglycaemic response to stimulation of the peripheral ends of the splanchnic nerves in adrenalectomized dogs and cats is directly dependent upon activation of sympathetic efferent fibres to the liver.     

Comparison of the hyperglycaemic and glycogenolytic responses to catecholamines with those to stimulation of the hepatic sympathetic innervation in the dog

1. The effects of stimulation of the splanchnic innervation to the adrenal medullae, in dogs with cut hepatic nerves, were compared with those obtained previously in response to splanchnic and hepatic nerve stimulation in adrenalectomized dogs.2. Maximal stimulation of both adrenal medullae via the splanchnic innervation (20 c/s for 9 min), in dogs with cut hepatic nerves, produced closely similar hyperglycaemic and glycogenolytic responses to those obtained previously in adrenalectomized dogs with intact hepatic nerves.3. The rise in plasma glucose concentration in response to maximal stimulation of the adrenal medullae in dogs with intact hepatic nerves was found to be comparable to that which occurs in response to maximal stimulation of the hepatic sympathetic innervation alone. In contrast, the rise in haematocrit during maximal stimulation of the entire splanchnic innervation was substantially greater than that observed after removal of both adrenal glands.4. The output of adrenaline and noradrenaline from the left adrenal gland was determined during maximal stimulation of the left splanchnic nerve (20 c/s for 9 min). These results were then used to compute doses of the two amines which would reproduce the output of catecholamines from both glands under such conditions. The extent of the rise in mean plasma glucose concentration in response to these infusions was similar to that produced by maximal stimulation of both adrenal glands, but the duration of hyperglycaemia and depletion of liver glycogen were significantly less.5. Stimulation of the splanchnic innervation was found to produce an initial ;surge' in the release of catecholamines from the adrenal medullae, followed by a rapid decline in output when stimulation was continued for longer than 30 sec. Evidence was obtained which showed that this pattern of release is well suited to produce rapid mobilization of liver glycogen.6. Comparable changes in plasma glucose concentration occurred in response to stimulation of either the adrenal medullae or the sympathetic innervation to the liver at low frequency (2.0 c/s for 5 min). Stimulation of both pathways simultaneously, at the same frequency, produced smaller responses.7. Intramesenteric infusions of noradrenaline at 1.0 mug.kg(-1) min(-1) for 5 min produced comparable changes in plasma glucose concentration to those observed during stimulation of either pathway alone at low frequency. The mean plasma noradrenaline concentration of portal blood was raised by between 92 and 105 ng/ml. during these infusions.8. It is concluded that stimulation of either the splanchnic innervation to the liver, or of both adrenal medullae, at high frequency (20 c/s for 9 min) represents a supramaximal stimulus for hepatic glycogenolysis. Comparison of the responses to stimulation at low frequency (2.0 c/s for 5 min) suggests that the hepatic glycogenolytic mechanism is equally sensitive to stimulation via either route in this species.     

The sensitivity of the hepatic glycogenolytic mechanism to stimulation of the splanchnic nerves

1. The sensitivity of the hepatic glycogenolytic mechanism to splanchnic nerve stimulation at relatively low frequencies has been investigated in adrenalectomized calves, dogs and cats.2. In young calves the hyperglycaemic response to splanchnic nerve stimulation at 1.0 c/s for 5 min increased steadily during the first 2 weeks after birth.3. The hyperglycaemic response to splanchnic nerve stimulation for 5 min was directly related to frequency of stimulation within the range 0.5-4.0 c/s in calves tested 2-5 weeks after birth. Pronounced rises in plasma glucose concentration also occurred in calves of this age in response to maximal stimulation (20 c/s) for shorter periods (30 sec) whereas occlusion of the portal vein for the same period produced no comparable effect.4. The effects of splanchnic nerve stimulation for prolonged periods were also investigated in 2- to 5-week-old calves. Under these conditions increased concentrations of glucose in the plasma were maintained for periods of up to 90 min and fell towards the initial values when stimulation was discontinued.5. Prolonged stimulation of the peripheral ends of both splanchnic nerves at either 2.0 or 4.0 c/s produced a transient reversal of hypoglycaemia in calves pretreated with large doses of insulin; both the extent and duration of these responses were related to frequency of stimulation.6. The hyperglycaemic response to bilateral splanchnic nerve stimulation was directly related to frequency of stimulation within the range 0.5-4.0 c/s in adrenalectomized dogs. Comparable responses were obtained in adrenalectomized cats in response to stimulation at 2.0 c/s, but stimulation at 1.0 c/s produced no rise in mean plasma glucose concentration in these animals.7. The sensitivity of the hepatic glycogenolytic mechanism has been assessed in relation to the associated changes in haematocrit and mean aortic blood pressure under the same conditions.8. The results of these experiments support the contention that tonic changes in sympathetic efferent activity are associated with variations in the rate at which glucose is released from the liver under physiological conditions.     

The release of pancreatic glucagon and inhibition of insulin in response to stimulation of the sympathetic innervation.

The changes in the concentration of glucagon and insulin in arterial plasma which occur in response to splanchnic nerve stimulation have been investigated in adrenalectomized dogs, cats and sheep. 2. In dogs, stimulation of both splanchnic nerves at a low frequency (2-0 c/s) for 10 min produced a small but statistically significant increase in plasma glucagon concentration and appeared to inhibit the release of insulin. Stimulation at a higher frequency (10-0 c/s) produced a much greater increase in plasma glucagon concentration, which was normally accompanied by a rise in plasma glucose concentration. 3. Qualitatively similar changes in plasma glucagon and insulin concentration were observed in both sheep and cats in response to adrenergic stimulation. 4. Intramesenteric infusions of glucagon at a dose of 5-0 ng kg-1 min-1 in dogs produced a comparable rise in plasma glucagon concentration to that elicited by splanchnic nerve stimulation at high frequency (10-0 c/s) and invariably caused a rise in plasma glucose concentration. 5. In dogs given exogenous glucose, release of glucagon in response to splanchnic nerve stimulation was unaffected by induced hyperglycaemia. Secretion of insulin was partially inhibited by stimulation at 2-0 c/s and completely suppressed at higher frequency (10-0c/s). 6. It is concluded that stimulation of the sympathetic innervation to the pancreatic islets, at frequencies within thephysiological range, stimulates the release of glucagon and inhibits that of insulin in each of these species.     

The glycogenolytic response to stimulation of the splanchnic nerves in adrenalectomized calves, sheep, dogs, cats and pigs

1. The effects of stimulation of the peripheral ends of one or both splanchnic nerves have been investigated in calves, sheep, dogs, cats and pigs after removal of both adrenal glands.2. Stimulation of both splanchnic nerves produced comparable hyperglycaemic and glycogenolytic effects in sheep, dogs and cats; the mean liver glycogen concentration was reduced by between 7.0 and 10.5 mg/g, five min after stimulation was discontinued, at which time the mean plasma glucose concentration had risen by between 126 and 137 mg/100 ml.3. In five 3-5 week-old calves which were tested under identical conditions the mean liver glycogen concentration was reduced by 13.3 +/- 1.9 mg/g and the plasma glucose concentration raised by 216 +/- 1.9 mg/100 ml., 5 min after stimulation was terminated.4. In pigs, stimulation of both splanchnic nerves invariably produced a rise in the plasma glucose concentration, even when the concentration of glycogen in the liver was less than 5 mg/g before stimulation. The response was, nevertheless, considerably smaller in these animals than in any of the other species investigated.5. Splanchnic nerve stimulation also caused a rise in mean aortic blood pressure and blood haematocrit during the period of stimulation; changes of approximately the same order of magnitude were encountered in all five species.6. Dogs were found to resemble calves in that the hyperglycaemic response to stimulation of a single splanchnic nerve did not differ significantly from that obtained when both were stimulated simultaneously; furthermore, either nerve was found to be equally effective.7. In cats the change in plasma glucose concentration in response to stimulation of a single splanchnic nerve was always less than that which occurred in response to bilateral stimulation although comparable changes in blood haematocrit occurred in both groups of animals.8. It is concluded that stimulation of the splanchnic nerves causes break-down of glycogen in the livers of various unrelated species of adult animals but that the magnitude of the hyperglycaemic response in the young calf provides further evidence of the importance of the sympathetic system in the control of metabolism in the young animal.     

Role of the Symphato-Adrenal System in Hemorrhagic Hyperglycemia

Arterial and venous plasma glucose concentration was determined at intervals in cats subjected to hemorrhagic hypotension at 50 mm Hg. The rapid rise of arterial plasma glucose after hemorrhage could be. attributed to an increased release of glucose from the liver. This hyperglycemia could not be eliminated by bilateral adrenalectomy or by sectioning of the hepatic sympathetic nerves, although the response was somewhat depressed by the latter procedure. On the other hand the hyperglycemia was virtually abolished after adrenalectomy when combined with bilateral sectioning of the major and minor splanchnic nerves. The level of plasma glucagon during hemorrhage increased in cats with an intact sympatho-adrenal system, but was unchanged in animals with combined splanchnic sympathectomy and adrenalectomy. It is concluded that, during hemorrhage, the sympatho-adrenal system influences the glucose output from the liver by three different reflex mechanisms: (a) release of catecholamines from the adrenal glands; (b) direct sympathetic nerve influence on the liver; and (c) release of glucagon from the pancreas.     

Role of the symphato-adrenal system in hemorrhagic hyperglycemia.

Arterial and venous plasma glucose concentration was determined at intervals in cats subjected to hemorrhagic hypotension at 50 mm Hg. The rapid rise of arterial plasma glucose after hemorrhage could be attributed to an increase release of glucose from the liver. This hyperglycemia could not be eliminated by bilateral adrenalectomy or by sectioning of the hepatic sympathetic nerves, although the response was somewhat depressed by the latter procedure. On the other hand the hyperglycemia was virtully abolished after adrenalectomy when combined with bilateral sectioning of the major and minor splanchnic nerves. The level of plasma glucagon during hemorrgage increased in cats with an intact sympatho-adrenal system, but was unchanged in animals with combined splanchnic sympathectomy and adrenalectomy. It is concluded that, during hemorrhage, the sumpatho-adrenal system influences the glucose output from the liver by three different reflex mechanisms: (a) release of catecholamines from the adrenal glands; (b) direct sympathetic nerve influence on the liver; and (c) release of glucagon from the pancreas.     

The glycogenolytic response to stimulation of the splanchnic nerves in adrenalectomized calves

1. The effects of stimulation of the peripheral ends of one or both splanchnic nerves have been investigated in adrenalectomized calves at different ages.

2. During the first 24 hr after birth unilateral splanchnic nerve stimulation led to a prompt rise in the plasma glucose concentration and this response was more than doubled when both nerves were stimulated simultaneously. Under these latter conditions hyperglycaemia was found to be associated with a measurable loss of glycogen from the liver.

3. Both the glycogenolytic and hyperglycaemic effects of splanchnic stimulation became more pronounced with age; at 5 weeks of age liver glycogen was depleted by approximately 2/3 and plasma glucose raised by about 200 mg/100 ml. after stimulation of the right splanchnic nerve for 9 min.

4. Splanchnic stimulation also caused a rise in mean arterial blood pressure and haematocrit during the period of stimulation at all ages studied; the rise in haematocrit was greatest in the oldest animals.

5. The hyperglycaemic response to splanchnic stimulation persisted after pancreatectomy and was also demonstrated in calves in which the whole of the portal effluent blood flow was collected during splanchnic stimulation. The plasma from blood collected in this way had no apparent hyperglycaemic effect when infused into a branch of the mesenteric vein in recipient calves.

6. In adrenalectomized calves in which the liver had been partially denervated before stimulation both the hyperglycaemic and the glycogenolytic responses were substantially reduced, although the rise in haematocrit was unaffected, during stimulation of both splanchnic nerves.

7. It is concluded that glycogenolysis occurs in the liver as a result of stimulation via the hepatic innervation in the new-born calf and that this response increases with age during the first few weeks after birth.

     

Nervous control of pancreatic exocrine secretion in pigs.

The pancreatic secretion of fluid, bicarbonate and protein in response to electrical stimulation of the vagus and splanchnic nerves, to exogenous and endogenous secretin and to various pharmacological agents was studied in anesthetized young pigs (21 kg). Vagal stimulation increased flow, bicarbonate output and protein output in a frequency dependent manner; the half maximal effective frequency was 2--4 Hz and the maximal effective frequency 12 Hz. The secretory response to vagal stimulation was potentiated by physiological elevations of the arterial concentration of secretin brought about by injection of secretin or by acidification of the duodenal bulb. Simultaneous stimulation of the splanchnic nerves strongly inhibited the response to vagal stimulation; splanchnic nerve stimulation alone had no demonstrable effect. The flow and bicarbonate response to vagal stimulation was unaffected by atropine, but abolished by hexamethonium. Protein output was strongly inhibited by both agents. The response to intraarterial infusion of acetylcholine resembled that elicited by vagal stimulation but it was smaller and it was completely abolished by atropine and unaffected by hexamethonium. Alpha- and beta-adrenergic blockade stimulated rather than inhibited the secretory response to vagal stimulation. The portal vein plasma concentration of secretin was not affected by vagal stimulation. The results indicate that the protein response, and the flow and bicarbonate response to vagal stimulation are not brought about by the same mechanism. An increased release of secretin is not involved. Peptidergic (VIP-containing) nerves may contribute.     

Distribution and possible origins of substance P-containing nerve fibers in the rat liver.

The distribution and possible origins of substance P-containing nerve fibers in the rat liver were investigated by immunohistochemistry and nerve transection. Nerve fibers with substance P-like immunoreactivity formed a more complex network than previously known in the walls of portal vein branches. Substance P-immunoreactive fibers were seen not only in and around the walls of the hepatic artery, but also in close association with the hepatic veins and bile ducts. Transection of the greater splanchnic nerves and/or the vagus nerves indicated that substance P-immunoreactive fibers in the walls of the portal and hepatic veins enter the liver via both nerves, and that those associated with the hepatic artery and bile ducts stem from the greater splanchnic nerves. The widespread distribution of hepatic substance P and its complex innervation pattern within the liver suggest that it is involved in a variety of physiological processes in this organ.     

Some data on intestinal paresis in experimental peritonitis

Summary Disturbances of the vegetative system control of the small intestine motor activity were studied in dogs with a parallel investigation of the blood neuromediators in conditions of expermental fecal peritonitis. The following was established: a reduction of the acetylcholine level, of the cholinesterase activity and a rise of adrenalin content from the 2nd to the 4th day with a gradual normalization by the 10th–12th day. The period of the greatest acetylcholine metabolism disturbance coincided with the loss of the effect produced by the vagus nerves and by the posterior spinal cord roots on the intestinal motor function. This effect is partially restored by administration of pharmacological acetylcholine. The inhibitory effect of the splanchnic nerves is retained at these periods of peritonitis development. Thus disturbed vegetative control of the intestinal motor function in conditions of peritonitis plays an important role in the development of the intestinal wall paresis.(Presented by Active Member of the Akad. Med. Nauk SSSR A. V. Lebedinskii) Translated from Byulleten' Éksperimental'noi Biologii i Meditsiny, Vol. 52, No. 10, pp. 54–57, October, 1961.     

Branches of the thoracic sympathetic trunk in the human fetus

Summary The segmental organization of the thoracic sympathetic trunk and all its ramifications was studied in 6 human fetuses (16–22 weeks) by means of the acetylcholinesterase in toto staining method. Each trunk was divided into 12 sympathetic segments. A segment is defined as that part of the sympathetic trunk which is connected via its rami communicates with one spinal nerve, without discriminating between grey and white rami. The diameter of the rami communicantes and their direction towards the spinal nerves are variable. The number of peripheral segmental ramifications of the trunk is much larger than assumed previously. Each thoracic sympathetic segment gives off at least 4–5 nerves. Three categories of nerves are discerned: (1) large splanchnic rootlets confined to the greater, lesser and least thoracic splanchnic nerves, (2) medium-sized splanchnic nerves directed towards thoracic viscera, some of which give off branches towards costovertebral joint plexuses and, described for the first time in man, (3) small nerves which ramify extensively and form nerve plexuses in the capsule of the costovertebral joints. The majority of the ramifications is formed by the nerves of the third category. The existence of Kuntz's nerve, connecting the 2nd intercostal nerve and 1st thoracic spinal nerve, is confirmed in four specimens. The nerve plexuses of the costovertebral joints receive a segmentally organized innervation: they receive their input from the neighbouring sympathetic segment and the one cranial to it.It is concluded that the thoracic sympathetic branches in man show a complex, segmentally organized pattern and may have a considerable component of somatosensory nerve fibers. The complex relationships must be taken into account in surgical sympathectomies.     

Nervous control of pancreatic exocrine secretion in pigs

The pancreatic secretion of fluid, bicarbonate and protein in response to electrical stimulation of the vagus and splanchnic nerves, to exogenous and endogenous secretin and to various pharmacological agents was studied in anesthetized young pigs (21 kg). Vagal stimulation increased flow, bicarbonate output and protein output in a frequency dependent manner; the half maximal effective frequency was 2–4 Hz and the maximal effective frequency 12 Hz. The secretory response to vagal stimulation was potentiated by physiological elevations of the arterial concentration of secretin brought about by injection of secretin or by acidification of the duodenal bulb. Simultaneous stimulation of the splanchnic nerves strongly inhibited the response to vagal stimulation; splanchnic nerve stimulation alone had no demonstrable effect. The flow and bicarbonate response to vagal stimulation was unaffected by atropine, but abolished by hexa-methonium. Protein output was strongly inhibited by both agents. The response to intraarterial infusion of acetylcholine resembled that elicited by vagal stimulation but it was smaller and it was completely abolished by atropine and unaffected by hexamethonium. Alpha- and beta-adrenergic blockade stimulated rather than inhibited the secretory response to vagal stimulation. The portal vein plasma concentration of secretin was not affected by vagal stimulation. The results indicate that the protein response, and the flow and bicarbonate response to vagal stimulation are not brought about by the same mechanism. An increased release of secretin is not involved. Peptidergic (VIP-containing) nerves may contribute.     

Comparison of the effects of hepatic nerve stimulation on arterial flow, distribution of arterial and portal flows and blood content in the livers of anaesthetized cats and dogs

1. The responses to hepatic nerve stimulation were studied in cats and dogs anaesthetized with sodium pentobarbitone. In three series of experiments, hepatic arterial flow was recorded by an electromagnetic flowmeter, intrahepatic distributions of arterial and portal flows were studied by radioactive microspheres, and hepatic volume responses were measured by a plethysmographic method.2. In cats, nerve stimulation produced a frequency-dependent decrease in hepatic arterial flow which was not maintained and autoregulatory escape occurred. In dogs, the initial decrease in arterial flow was similar but escape did not occur and the vasoconstriction was well maintained.3. In both cats and dogs, stimulation of the hepatic nerves did not cause a redistribution of either arterial or portal flows within the liver. Autoregulatory escape in the liver of the cat was not associated with an intrahepatic redistribution of arterial flow and is best interpreted as relaxation of the same vessels which were initially constricted, due to increased production of a vasodilator factor.4. Stimulation of the hepatic nerves caused a marked frequency-dependent decrease in hepatic volume which was well maintained and the responses were similar in cats and dogs. The quantitative importance of the liver as a blood reservoir is compared in relation to other vascular beds and the concept of the blood volume reserve is discussed.     

Secretion from the Dog's Parotid at Different Time Intervals after Denervation

Previous observations suggest that cholinergic secretory fibres reach the dog's parotid gland not only via the auriculo-temporal nerve but also along the internal maxillary artery. 3–5 days after section of both these sets of nerves citric acid applied to the oral mucosa was found to evoke slow secretion only, or none at all. It has been reported, however, that the secretory response elicited reflexly after auriculo-temporal nerve section gradually increases during the days following the operation. The auriculo-temporal nerve was divided unilaterally in one group of dogs, and in another group this operation was combined with section of the nerves on the internal maxillary artery. During the following five weeks the dogs were examined repeatedly. Each time the secretory innervation was studied in two ways: by pouring citric acid into the mouth and by injecting esenne through the salivary duct into the gland. In addition the secretory responses to methacholine were estimated. The results indicate that postoperatively there was first a period in which there wag some increased release of acetylcholine in the gland (a “degeneration phenomenon”); supersensitivity then developed in the secretory cells. In spite of these complications both methods to study the secretory innervation could be used after the first week and onwards to demonstrate the difference in the effectiveness between the two denervation procedures.     

Spinal autonomic afferents in elicitation of tachycardia in volume infusion in the dog.

Intravenous infusion of blood (36 ml/kg body wt) elicited tachycardia in artificially ventilated anesthetized dogs with intact autonomic innervation and in dogs with cardiac beta-receptor blockade. In contrast, infusion elicited bradycardia in dogs with section of the spinal cord at C6-C7, and in dogs with combined spinal section and cardiac beta-receptor blockade. The control heart rate was less than or equal to 110 beats/min in all the animals. The presence of infusion-induced tachycardia in dogs with beta-receptor blockade, i.e., dogs in which cardiac sympathetic efferents were blocked, and its absence in dogs with combined spinal section and beta-receptor blockade, i.e., dogs in which spinal autonomic afferents plus cardiac sympathetic efferents were blocked, may be the result of an additional interruption of spinal autonomic afferents by spinal section. It is concluded that tachycardia elicited by infusion may be partly due to a reflex with its afferent pathway in the spinal cord and its efferent pathway in the vagus nerves.     

On the sympathetic innervation to the cat's liver and its role for hepatic glucose release

Morphology and function of the adrenergic innervation of the liver were studied in cats. Fluorescence microscopy revealed a dense network of adrenergic nerve fibres in association with interlobular vessels and a sparse, but unequivocal innervation of the hepatocytes. These parenchymal adrenergic nerve fibres were more frequent in kittens (2 months old) than in adult cats. Electrical stimulation of the hepatic sympathetic nerves in the adult adrenalectomized cat evoked a small but insignificant increment (1–2 mM) of arterial plasma glucose concentration. When both hepatic and pancreatic sympathetic nerves were stimulated simultaneously, arterial plasma glucose concentration increased significantly by about 6 mM. We conclude that the pronounced hyperglycemic effect of activation of the sympathetic nervous system in the cat is mediated mainly via an adrenergic influence on the release of insulin and glucgon from the pancreas. The sympathetic innervation of the cat liver parenchyma seems to contribute to the hyperglycemia to a minor extent only.     

Direct neural inhibition of insulin secretion in response to systemic hypoglycemia.

The innervated pancreas of an anesthetized small "pancreas" dog was cross-perfused with blood from a large "support" dog in order to separate neural from blood-borne influences on the immunoreactive insulin secretion rate (ISR). The arterial plasma reducing sugar (sugar) concentration could be varied independently in the pancreas dog systemic circulation and in its pancreas. After tying of the hepatic arteries and portal vein in the pancreas dog, its systemic arterial plasma sugar concentration was allowed to fall in 10 experiments. This was prevented in five control experiments by intravenous glucose infusion (7 mg/kg-min). In all experiments, pancreatic arterial plasma sugar concentration was sustained, and at 40 min it was elevated 50 mg/100 ml by glucose infusion into the pancreatic blood supply. Bilateral splanchnic nerve section at 120 min caused an increase of the ISR in all experiments, but a greater rise occurred from the pancreases of the 10 dogs allowed to become hypoglycemic (P less than .02). In two further experiments, the splanchnic nerves were not cut, and no rise in ISR occurred. In conclusion, systemic hypoglycemia can inhibit insulin secretion by means of the splanchnic nerves.     

The functional morphology of the afferent systems of the splanchnic nerves

Summary The morphology, the sources of formation and the functional characteristics of the afferent sympathetic fibers of the splanchnic nerves were studied.The removal of the gall bladder and of the small intestine, as well as of the semilunar ganglia of the solar plexus was associated with a secondary degeneration of the amyelinated and thin myelinated conductors contained in the splanchnic nerves. This fact shows that they pertain to the neurites of the receptor neurons (II type Dogiel's cells) located in the plexuses within the walls of the corresponding organs.The electrophysiological and the histochemical study of these neurites was studied after the exclusion of all the spinal afferent fibers of the splanchnic nerves. The preservation of their morphology, function and the enzymatic activity in the peripheral portion of the splanchnic nerve in 21–27 days after its section was demonstrated. Their physiological characteristics are determined by the functional, state of the corresponding organ.Presented by Active Member AMN SSSR V.N. ChernigovskiiA paper presented to the First Belorussian Conference of Anatomists, Histologists, Embryologists and Topographical Anatomists on June 14, 1957, in Minsk.     

Efferent paths of the esophago-intestinal reflex

Summary It was shown that in chronically esophagotomized dogs, when the splanchnic nerves are left intact, the excitatory effect on movements of the small intestine produced by esophageal stimulation are eliminated by bilateral transdiaphragmal vagotomy, but are still present if the vagi are left intact and the splanchnic nerves divided. After division of both the vagi and the splanchnic nerves, stimulation of the esophagus does not influence movements of the small intestine. In animals with divided vagi and intact splanchnic nerves, pronounced inhibition of intestinal movements is caused by esophageal stimulation whereas when both vagus and splanchnic nerves are intact, the inhibition seldom occurs and it is thought that the reason for the failure is the prevalence of the excitatory effect of esophageal stimulation. It is concluded that the excitatory effect from the esophagus (esophagointestinal reflex) is transmitted through the vagi, and the inhibitory influences through the sympathetic nerves.(Presented by Active Member AMN SSSR V. I. Chernigovskii) Translated from Byulleten Èksperimental' noi Biologii i Meditsiny Vol. 49, No. 4, pp. 24–27, April, 1960