Vagal Gastric Secretory Nerves in the Rat Demonstrated With Insulin

1957 ◽  
Vol 191 (2) ◽  
pp. 262-264 ◽  
Author(s):  
Ardelle Lane ◽  
A. C. Ivy ◽  
E. K. Ivy
Keyword(s):  
Gastric Secretion ◽  
Secretory Response ◽  
Gastric Fistula ◽  
Vagus Nerves ◽  
Insulin Hypoglycemia

It was found in four tests on each of 12 rats with a chronic gastric fistula and accustomed to the experimental procedures that insulin hypoglycemia short of convulsions stimulated gastric secretion when the vagus nerves were intact. In five tests on each of seven rats, it was found that section of the vagi abolished the secretory response to insulin hypoglycemia. This evidence is interpreted as establishing the presence of gastric secretory nerves in the vagi of the rat.

Alterations in gastric secretion following hypothalamic lesions producing hyperphagia

1965 ◽  
Vol 209 (2) ◽  
pp. 319-323 ◽  
Author(s):  
Peter T. Ridley ◽  
Frank P. Brooks
Keyword(s):  
Food Intake ◽  
Gastric Secretion ◽  
Neural Control ◽  
Neural Mechanisms ◽  
Gastric Fistula ◽  
Central Regulation ◽  
Pepsin Secretion ◽  
Insulin Hypoglycemia ◽  
Hypothalamic Lesions

Fasting gastric secretion and secretion during insulin hypoglycemia were collected from hypothalamic hyperphagic rats equipped with chronic gastric fistula in an attempt to correlate the hypothalamic neural mechanisms controlling food intake with gastric secretion. The interdigestive or basal fasting secretion of rats rendered hyperphagic by stereotaxic ablation of the ventromedial nuclei was significantly increased in volume, acid concentration and output, and pepsin output when compared with control and sham-operated rats and rats with hypothalamic lesions without hyperphagia. Hypothalamic hyperphagic rats did not show a significant increase in gastric secretion during insulin hypoglycemia, whereas the other groups did. The levels of hypoglycemia induced by insulin were comparable in all groups. These studies suggest an important role of the ventromedial nuclei in the central regulation of acid and pepsin secretion, and also relate the hypothalamic neural control of gastric secretion to that of food intake. The results also indicate that this nucleus is involved either as a "center" or pathway in the augmentation of gastric secretion by insulin hypoglycemia.

Gastric Secretion and Free Histamine in Urine

1958 ◽  
Vol 195 (1) ◽  
pp. 202-208 ◽  
Author(s):  
William T. Irvine ◽  
Charles F. Code
Keyword(s):  
Gastric Secretion ◽  
Gastric Juice ◽  
Free Acid ◽  
Secretory Response ◽  
Active Secretion ◽  
Insulin Hypoglycemia ◽  
Urinary Histamine ◽  
Made In

Simultaneous determinations of the hourly outputs of free histamine in the urine and free acid in the juice from Heidenhain gastric pouches were made in dogs after the ingestion of meat. The gastric secretory response to the meal was separated into intestinal and gastric components. The rough parallelism, noted by others, between the outputs of acid in the gastric juice and free histamine in the urine after the meal was verified. When the meat was placed in the jejunum the output of histamine in the urine promptly increased while the output of acid was minimal or absent. Later, the output of acid increased while the output of histamine declined. Meat placed in the isolated stomach produced active secretion of acid but no increase in urinary histamine. No increase of urinary histamine followed a meal of bread and milk. During nervous secretion induced by insulin hypoglycemia, the output of free histamine in the urine did not change.

Effects of bombesin on food intake and gastric acid secretion in cats

1989 ◽  
Vol 256 (1) ◽  
pp. R181-R186
Author(s):  
A. Bado ◽  
M. J. Lewin ◽  
M. Dubrasquet
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Gastric Secretion ◽  
Acid Secretion ◽  
Gastric Fistula ◽  
Single Class ◽  
Heidenhain Pouch ◽  
Daily Food Intake ◽  
Feeding Experiments ◽  
Daily Food

The brain and gut peptide bombesin has been reported both to stimulate gastric secretion and to induce satiety. To understand how the peripheral administration of bombesin affects food intake and whether gastric mechanisms are involved, a comparative study of the doses of bombesin active on gastric secretion, gastric emptying, and food intake was undertaken in cats provided with a gastric fistula and a denervated Heidenhain pouch. The smallest dose of intravenous bombesin that stimulated significantly basal acid secretion (20 pmol.kg-1.h-1) by the gastric fistula also enhanced meal-stimulated acid secretion by the Heidenhain pouch (+138%, P less than 0.01), delayed gastric emptying of a liquid protein meal (-30%, P less than 0.01), and suppressed food intake when the test meal was allowed to reach the stomach (-15%, P less than 0.01). Conversely, in sham-feeding experiments, the same dose of bombesin increased food intake (+35%, P less than 0.01). In full-day experiments conducted in nonfasted cats, bombesin decreased both the food intake in the 4-h period after the infusion and the daily food intake, whereas octapeptide cholecystokinin induced a transient satiety but did not decrease daily food intake. These results indicate that in cats the interaction of bombesin with "pregastric" mechanisms is not sufficient to induce satiety and that a relation could exist between the effects of bombesin on gastric secretion, emptying, and food intake. A single class of receptors might be involved in these peripheral effects of bombesin.

Gastric Secretion Following Vagosplanchnic Nerve Anastomosis

1956 ◽  
Vol 184 (2) ◽  
pp. 418-427 ◽  
Author(s):  
Anthony M. Imparato ◽  
L. Corsan Reid ◽  
J. William Hinton
Keyword(s):  
Electrical Stimulation ◽  
Gastric Secretion ◽  
Functional Relationship ◽  
Early Postoperative Period ◽  
Insulin Hypoglycemia ◽  
Splanchnic Nerves ◽  
Nerve Anastomosis ◽  
Nerve Anastomoses ◽  
Secretory Apparatus ◽  
Stimulation Of

Gastric secretion in response to insulin hypoglycemia and electrical stimulation of the vagus was studied in 18 dogs who had bilateral vagosplanchnic anastomoses in the chest. In six dogs the pattern of gastric secretory response to insulin changed from negative in the early postoperative period to positive between 85 and 613 days postanastomosis. In two, apparent return of vagus function was confirmed by electrical stimulation of the vagi. One of five dogs in whom splanchnovagal nerve anastomoses were performed showed a return of response to insulin at 63 days which was abolished by excision of the anastomoses. On the basis of a review of some of the ideas regarding interpretation of cross nerve anastomoses and some of the conflicting opinions regarding the fiber content of the sympathetic splanchnic nerves, the authors conclude the most likely explanation for the observed phenomena is that there are preganglionic cholinergic fibers in the greater splanchnic nerves whose relationship to the gastric secretory apparatus is similar to that of cholinergic fibers in the vagus. The regenerating fibers of the vagus followed the sheaths of these degenerating fibers and re-established functional relationship with the gastric secretory apparatus.

Control of bile flow in the cholecystectomized dog

1963 ◽  
Vol 204 (5) ◽  
pp. 825-828 ◽  
Author(s):  
Michael E. Fritz ◽  
Frank P. Brooks
Keyword(s):  
Bile Flow ◽  
Anticholinergic Drug ◽  
Vagus Nerves ◽  
Intestinal Hormones ◽  
Insulin Hypoglycemia ◽  
Intravenous Insulin ◽  
Bilateral Vagotomy ◽  
The Common ◽  
Choleretic Effect

Rate of flow and composition of bile were measured in three unanesthetized, cholecystectomized dogs. One of these animals and one other dog were also studied after bilateral vagotomy. Bile flow and output of solids were increased by intravenous insulin and feeding. Tolbutamide had a similar choleretic effect. The anticholinergic drug, pipenzolate methylbromide blocked the choleretic effect of insulin. After bilateral vagotomy, the choleretic effect of both feeding and insulin-hypoglycemia was lost. Commercial pancreozymin had a choleretic action which may indicate a role of intestinal hormones in the response to feeding. Intraduodenal injection of hydrochloric acid was followed by an increase in only the volume of bile. Glucagon produced a hydrochloresis and an increase in bilirubin output. The results suggest that normal bile production in the dog after eating may be controlled in part by a mechanism involving the vagus nerves. The data also show that the insulin-hypoglycemia-induced choleresis differs from that of secretin. The composition of hepatic bile obtained from the common duct is consistent with an absorptive function of the ductal epithelium in the dog without a gallbladder.

Motility studies of isolated antral pouches before and after vagus denervation

1959 ◽  
Vol 14 (1) ◽  
pp. 22-26 ◽  
Author(s):  
Donald E. Wohlrabe ◽  
William D. Kelly
Keyword(s):  
Electrical Stimulation ◽  
Reliable Method ◽  
Time Interval ◽  
Vagus Nerves ◽  
Parasympathetic Innervation ◽  
Insulin Hypoglycemia ◽  
Difference Of Opinion ◽  
Before And After ◽  
Vagal Innervation ◽  
Greater Curvature

The motility responses of vagus innervated and denervated antral pouches to electrical stimulation of the vagus nerves and to insulin hypoglycemia were determined. Electrical stimulation appears to be a reliable method of demonstrating the presence or absence of vagus nerve supply to the antrum both in acute studies and in preparations of several months' duration. The motility response of the antral pouch to insulin hypoglycemia was found to be a less reliable method of determining the presence or absence of vagal innervation largely because spontaneous hypermotility may occur and there is more room for difference of opinion in interpretation of the results obtained. The administration of glucose after an appropriate time interval, however, added significantly to the reliability of the test. By the methods employed the antral branches of the vagus nerves were found to be the only sources of vagus innervation of the antrum. No evidence was obtained to suggest effective parasympathetic innervation of the antrum via a pyloric nerve, via the greater curvature mesenteric attachment or via an intramural gastric pathway. Submitted on July 7, 1958

Supra-Diaphragmatic Section of Vagus Nerves and Gastric Secretion in Patients with Peptic Ulcer

1945 ◽  
Vol 59 (2) ◽  
pp. 140-141 ◽  
Author(s):  
T. F. Thornton ◽  
E. H. Storer ◽  
L. R. Dragstedt
Keyword(s):  
Peptic Ulcer ◽  
Gastric Secretion ◽  
Vagus Nerves

Effect of antrectomy of gastric secretion induced by insulin hypoglycemia in dogs

1977 ◽  
Vol 83 (3) ◽  
pp. 298-301
Author(s):  
A. A. Fisher ◽  
Yu. M. Zubenko ◽  
R. I. Polyak
Keyword(s):  
Gastric Secretion ◽  
Insulin Hypoglycemia
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