Pouch Secretion Research Articles

Gastric dysfunction in sheep infected with Trichostrongylus colubriformis, a nematode inhabiting the small intestine

Barker I. K. and Titchen D. A. 1982. Gastric dysfunction in sheep infected with Trichostrongylus colubriformis, a nematode inhabiting the small intestine. International Journal for Parasitology 12: 345–356. Six of 12 lambs infected with Trichostrongylus colubriformis had reduced abomasal acidification (pH 4.0–8.1) in comparison with uninfected pair-fed and replete controls (pH <3.5), though less than 0.8% of the worm burden was in the abomasum. Loss of prominence of parietal cells and encroachment of mucous cells deep into fundic glands was seen by light microscopy. Under the electron microscope, parietal cells had little canalicular or tubulovesicular development, had large vacuoles, many polyribosomes and few mitochondria in comparison with those in controls. In a further 8 sheep prepared with abomasal fistulae and separated fundic pouches and inoculated orally with T. colubriformis, the volume of fundic pouch secretion declined as feed intake dropped and in 7 out of 8 animals H + concentration in fundic pouch secretion also fell. Infection generally reduced volume and acidity of pouch secretion more than did a pre-inoculation fast. In 5 sheep, abomasal content exceeded pH 4. Inoculation of T. colubriformis by enterotomy and Ostertagia circumcincta per os, in a lamb with a separated fundic pouch, caused depression of volume and acidity of pouch secretion characteristic of T. colubriformis infection, rather than the hypersecretion typical of abomasal infection with Ostertagia. Factors inhibitory to parietal cell differentiation and gastric acid secretion may be released from the small intestine of some sheep in response to changes in the gut induced by the presence of T. colubriformis. Abomasal dysfunction is a manifestation of severe intestinal trichostrongylosis.

Catecholamines and the cephalic phase of gastric secretion

Methoxamine, an α-adrenergic agent, and isoproterenol, a β-adrenergic agent, significantly augmented indirect vagally stimulated (intravenous 2-deoxy-D-glucose) acid and pepsin secretion from the main stomachs of conscious dogs. Heidenhain pouch secretion in the same dogs was unaffected.

Vasoactive intestinal peptide-associated inhibition of stimulated gastric secretion: II. Inhibition of pentagastrin-stimulated gastric secretion

The possible role of vasoactive intestinal peptide as an inhibitor of stimulated gastric secretion was investigated. Awake dogs with Heidenhain pouches were stimulated with pentagastrin alone and in combination with intraduodenal instillation of various potential inhibitors of gastrointestinal secretion including isotonic phenylalanine, 3 percent hypertonic saline solution and 0.16 normal hydrochloric acid. Plasma vasoactive intestinal peptide is significantly increased by pentagastrin, and this release is enhanced by intraduodenal hydrochloric acid. Simultaneously, there is significant inhibition of pentagastrin-stimulated Heidenhain pouch secretion. These findings provide evidence for a possible physiologic role of vasoactive intestinal peptide as an inhibitor of gastric secretion, at least in dogs.

Effect of an intravenous fat preparation on canine gastric secretion

The effect of intravenous administration of a fat emulsion on canine gastric secretion stimulated by intravenous infusion of amino acids, pentagastrin or insulin was studied. The fat preparation was given at a rate of 30 ml/hour for 2 hours, and its effects were compared with those of a comparable amount of saline solution, each given on three separate occasions in each dog. Fat did not alter the Heidenhain pouch secretion stimulated by intravenous amino acids (1.10 versus 1.11 mmol of hydrogen ion, p >0.9) or the gastrostomy secretion stimulated by intravenous insulin (9.22 versus 9.54 mmol of hydrogen ion, p >0.7) but had a modest inhibitory effect on Heidenhain pouch secretion stimulated by pentagastrin (2.75 versus 3.54 mmol of hydrogen ion, p <0.05). These data provide indirect support for the contention that the inhibition of gastric secretion by fat in the gut is mediated by the release of an enterogastrone rather than by a direct effect of absorbed fat. Because gastric stimulation by intravenous fat was not observed in the dog, it seems likely that intravenous fat emulsion can be given to seriously ill patients without fear of an increased likelihood of peptic ulceration due to induced gastric hypersecretion.

Vasoactive intestinal peptide inhibition of stimulated gastric secretion: I. Inhibition of meat-stimulated gastric secretion

In an effort to demonstrate a physiologic role of vasoactive intestinal peptide, awake dogs with either Heidenhain pouches or Thiry-Vella loops and duodenal cannulas with duodenoduodenostomies to prevent obstruction were stimulated with meat meals given by mouth and infusions of various substances given intraduodenally, including hypertonic saline solution or 0.16 normal hydrochloric acid. Stimulated Heidenhain pouch secretion was significantly inhibited by concomitant intraduodenal administration of hydrochloric acid. Plasma vasoactive intestinal polypeptide was highest in the animals who received hydrochloric acid intraduodenally among all the intraduodenal stimuli. These findings support a role for vasoactive intestinal polypeptide as a physiologic inhibitor of gastric secretion, at least in dogs.

Permeability effects of the E2 prostaglandins on canine gastric mucosa.

The effects on gastric mucosal permeability (GMP) of the topical application and intravenous administration of prostaglandin E2 (PGE2), 15(S)-15-methyl prostaglandin E2 (15M), and 16,16-dimethyl prostaglandin E2 (16DM) were measured in canine Heidenhain pouches. Two groups of four dogs were used and each experiment consisted of a 3-h perfusion with an acid saline solution containing polyethylene glycol as a volume marker. The prostaglandin was either added to the perfusate or given by constant intravenous infusion. The H+ and Na+ fluxes were used to assess GMP. Topical (1–10 μg/mL) and intravenous (0.3–1.2 μg kg−1 h−1) 16DM increased the apparent Na+ flux into the pouch in association with the secretion of fluid by the pouches, but did not alter H+ flux. The PGE2 applied topically (10–1000 μg/mL) had a similar effect, but intravenously (0.3–1.2 mg kg−1 h−1) reduced the volume of pouch secretion and the apparent Na+ flux into the pouch without altering H+ flux. The 15M given in the same concentration as 16DM was without a consistent effect on ionic flux or volume of secretion. The E2 prostaglandins have no effect on normal GMP.

Influence of the abdominal vagi and gastric antrum on humoral control of gastric acid secretion

AbstractThe influence of the abdominal vagi (especially the gastric antral branch), the antrum, and the duodenum on humoral control of gastric acid secretion was studied in 9 dogs with Heidenhain pouches (HP). The dogs were divided into 2 groups and subjected to the following sequential operations:Group I: (6 dogs) The first operation was section of the antral branch of the vagus nerve. The second operation was antrectomy with Billroth I gastroduodenostomy. The third operation was transthoracic truncal vagotomy.Group II: (3 dogs) The first operation was antrectomy and Billroth II gastrojejunostomy and the second operation was transthoracic truncal vagotomy. During the control period when the dogs had only an HP, pouch acid secretion and serum gastrin level increased after feeding. After antral vagotomy, both pouch secretion and the serum gastrin level after feeding were significantly lower. The second operation of antrectomy with Billroth I gastroduodenostomy in Group I resulted in a further significant decrease in both pouch acid secretion and serum gastrin level. Similar decreases occurred after the first operation of antrectomy with Billroth II gastrojejunostomy in Group II. In both groups, after the final operation of transthoracic truncal vagotomy, pouch acid secretion tended to increase, while the serum gastrin level increased slightly in Group I but not in Group II. It is concluded that vagal innervation of the antrum plays a role in gastrin release and gastric acid secretion.

On the Cause of the Increased Heidenhain Pouch Secretion and Serum Gastrin Concentration after Gastrojejunostomy in Dogs: With a statistical appendix

In 10 dogs with Heidenhain pouches (HP) a gastrojejunostomy (GEA) was constructed and later converted into a Roux en-Y anastomosis in order to abolish or reduce transstomal reflux. Next, duodenal inhibition was abolished by duodenal transection, and finally the duodenal bulb was excised. Twenty-four hour HP acid output increased after GEA, some 70% of the increase being attributable to transstomal reflux, the rest to decreased duodenal inhibition. Abolished duodenal inhibition caused a new rise, not significantly different from that caused by the combined effect of reflux and decreased duodenal inhibition after GEA. Twenty-four hour fasting HP acid output and 5 hr food-stimulated HP acid output rose after GEA by the same amount as that caused by abolished duodenal inhibition. A significant correlation was found between integrated gastrin and total HP acid output after food stimulation. Both fasting and food-stimulated gastrin concentration rose after GEA, the latter caused by reflux alone. Elimination of duodenal inhibition caused an unexpected rise in both fasting and food-stimulated gastrin concentration.

Effects of a series of infections of Ostertagia circumcincta on gastric secretion of sheep.

Sheep which had been either previously infected with 3. circumcincta or maintained worm-free, were surgically prepared with separated fundic pouches and abomasal cannulae and subsequently infected with 20,000 O. circumcincta larvae three times weekly. A reduction in food intake and increases in total acid output from the pouches and plasma pepsinogen levels were evident in both groups of sheep 4 days after repeated infections commenced; effects which increased in severity after 12 or more days. Except for a transient period of slight failure, previously infected sheep retained the capacity to acidify their abomasal contents whereas previously worm-free sheep lost this capacity. These changes were reversed between 2 and 7 days after treatment with thiabendazole (88 mg.kg-1). Secretory capacity of the fundic pouches was tested with histamine (40 mug.kg-1), the histamine antagonist (burimamide 8 mg.kg-1) and atropine (100 mug.kg-1). Ostertagiasis reduced or abolished the stimulatory effects of histamine. An increase in secretion volume and acid output was obtained after food was freshly provided, even though as little as 25 gm was consumed. Atropine and burimamide both caused a profound decrease in pouch secretion and acid output. These data are consistent with the hypothesis previously stated that in ostertagiasis the hypersecretion from fundic pouches is due to increased levels of circulating gastrin.

Gastric, antral and fundic pouch secretion in sheep.

1. Fundic secretion of HCl and pepsin was studied in sheep with both fundic and antral pouches. The antral pouches were of the entire pyloric region. Continuity of the alimentary tract was restored by an abomasoduodenal anastomosis. 2. Secretion from fundic pouches was continuous. It was reduced in volume and acidity, was pepsin output, by resection of the antral pouches. 3. Teasing with food, feeding and injection of pentagastrin stimulated fundic acid and pepsin secretion in animals with antral pouches before and after antrectomy. 4. Pouches prepared from the entire pyloric region showed continuous secretion with variations not related to feeding or fasting. Antral secretion was increased after s.c. injections of histamine, carbachol and pentagastrin. 5. It is concluded that although the pyloric antrum contributes to the magnitude of the secretory response of an abomasal fundic pouch, the direction of the secretory response is similar whether or not the pyloric antrum is present as a separated pouch, or is removed.

Parietal cell vagotomy in dogs. Influence on heidenhain pouch acid secretion, serum gastrin concentration, gastric emptying and motility.

No change was observed in fasting Heidenhain pouch (HP) acid secretion and fasting serum gastrin concentration following parietal cell vagotomy (PCV) in six dogs whereas significant increase in food-stimulated pouch secretion and serum gastrin concentration was observed. The increase in pouch secretion after PCV took place mainly in the first 2 h after meal. The maximum serum gastrin concentration was reached at 15 min after feeding before as well as after PCV. Maximum in HP secretion was reached later, at 120 min before and at 90 min after surgery. Gastric emptying studies, using a food-barium meal, showed a slight decrease in the emptying rate after PCV in two dogs, while it was unchanged in the others. Cineradiography showed an unaffected antral motility in all dogs after PCV.

Effects of the amount and type of food eaten on secretion from fundic abomasal pouches of sheep.

1. The effects on gastric secretion of altering the amount and type of food eaten were examined in sheep with fundic abomasal pouches and in sheep which also had the antral region of the abomasum isolated into a pouch or removed (antrectomy). Secretion, which was continuous in all preparations, was collected over 24 h periods, and daily determinations of its acid and pepsin concentrations were made for periods of up to 10 weeks.2. Experimental diets consisting of chaffed lucerne, meadow and wheaten hays were fed onad lib. or restricted regimens.3. Raising and lowering the dry matter (DM) intakes of lucerne chaff increased and decreased respectively the volume, acidity and acid and pepsin outputs (volume x concentration of acid or pepsin) of fundic pouch secretion.4. Increases of 27–64% in the amount of lucerne chaff eaten, after changing from restricted toad lib. feeding, were followed by increases in the volume (19–66%), acid concentration (4–10 mequiv. H+/l, 3–9%) and acid output (18–76%) of pouch secretion.5. With DM intakes of mixed lucerne and wheaten chaffs between 88 and 107% of those of lucerne, the secretion from the pouches was reduced to 45–88% of the volume and 39–77% of the acid output observed with the lucerne diet. Acid concentration was least affected, being unchanged in one series of observations and decreased by, at the most, 13 mequiv. H+/l (12%) in another. Reverting to a diet of lucerne chaff reversed these effects: the volume was increased by 30–49%, acid concentration by 2–15 mequiv. H+/l (2–14%), acid output by 38–68% and pepsin output by 30–43% although the intake of DM was the same or 6% less than that on the wheaten chaff mixture.6. Secretion was greater when animals ate lucerne chaff than when they ate meadow chaff.7. The changes in secretion according to diet were obtained in animals with antral pouches and antrectomy as well as in those with only fundic pouches.8. It is argued in discussion that the markedly different abomasal secretions on different diets arise from abomasal stimulation due to the nature rather than the amount of digesta entering it and that although the pyloric antrum contributes to these changes it is not essential for their occurrence.

The influence of bile on canine gastric secretion

The effect of various types of biliary diversion on the daily secretion of Heidenhain pouches in dogs was studied. Total external diversion of bile brought about a decrease in gastric secretion while simple internal diversion of bile to the distal gut via Roux-en-Y segment caused significant increase in Heidenhain pouch secretion; the observed increases in secretion could not be accounted for on the basis of impairment of liver function as measured by serial BSP determinations.

The effect of duodenal regurgitation into the canine stomach on gastric secretion

Submitted for publication December 8, 1972. THE POSSIBLE EFFECT OF DUODENAL REGURGITATION on gastric secretion has long attracted considerable interest. At the turn of the century Sokolov [19] observed increased secretion from Pavlov pouches after instillation of bile into the dog stomach. 1924 Meyer et a,Z. [13] recorded a moderate increase in the Pavlov pouch secretion after similar circumstances, especially if the pouch was already secreting. In 1936 Kim and Ivy [lo] used a total gastric pouch as measuring organ, t,hey found bile to be a mild stimulus for acid secretion, whereas pancreatic juice did not stimulate at all. Kaulbersz et al. [9] reported in 1942 that bile introduced into the stomach of dogs with Pavlov pouches increased the secretory response to histamine. In dogs with Heidenhain pouches bile failed to stimulate secretion. In 1944 Beamer et al. [l] . t d d th 1 in ro uce ra er arge volumes of bile into dogs with gastric and duodenal fistulas. They noted a secretion of gastric juice after a latent period of 30-45 min. Bile introduced into the duodenum stimulated gastric secretion only when it was allowed to regurgitate into the stomach. Again, the increase was not very large. In later years clinical observations on patients with gastric ulcer disease have placed much emphasis on regurgitation of

Effects on abomasal function of Ostertagia circumcincta infections in sheep.

Sheep in which abomasal fundic pouches had been made were infected with Ostertagia circumcincta (150000 larvae in one sheep, 100000 in three sheep). Subsequently studies were made on pouch secretion, food intake, plasma pepsinogens and abomasal pouch secretory responses when the sheep first ate. A functional abomasal lesion was apparent within 4 days of infection judged by the changes in plasma pepsinogen levels and the sodium concentrations of abomasal contents. Whereas the secretory activity of the abomasal fundic pouches (never exposed to parasites) was maintained or increased, the pH and sodium concentration of contents taken from the infected part of the abomasum were indicative of either a failure to secrete or of a permeability reabsorptive lesion. Ultrastructural studies demonstrated that parietal cells of the pouches had the appearance of cells subjected to strong secretory stimuli, but those of infected abomasa were similar to cells of gastric mucosa subjected to agents suppressing secretion. Factors which might operate, on the one hand, to stimulate secretion from separated fundic abomasal pouches, and on the other to inhibit or modify the secretory activity of the fundic mucosa of the infected abomasa, are discussed.

Comparative effects of aliphatic alcohols on the gastric mucosa.

SummaryWe studied the effects of a series of aliphatic alcohols on the gastric mucosa of Heidenhain pouches in four unanesthetized dogs. Transmucosal potential difference (PD). and the net fluxes of H+, Na+, and Cl–, were determined in the presence of various concentrations of methanol, ethanol, n-propanol, and t-butanol. Each alcohol caused a decrease in the PD and an increase in the net flux of Na+ ion into the lumen of the pouch. On a molar basis, t-butanol = n-propanol > ethanol > methanol in their effects on PD and net Na+ flux. Except for t-butanol there was a linear relationship between the ability of the alcohol to alter PD and the oil-water partition coefficient of the alcohol. Low concentrations of ethanol and n-propanol caused a net flux of H+ ion into the pouch (secretion). Higher concentrations of these alcohols and all concentrations of methanol and t-butanol caused a net loss of H+ ion from the pouch. The net flux of Cl- ion tended to parallel and equal the net flux of cations.We conclude t...

Pancreatectomy and liver damage: effects on humoral gastric secretion in dogs.

Twelve Heidenhain pouch dogs were examined for pancreatic and hepatic effects on humoral gastric secretion. In three dogs pancreatin and methionine given orally did not change pouch output of acid. Total pancreatectomy was performed in the remaining nine dogs. In three dogs pancreatin and methionine were given immediately after surgery to prevent fatty metamorphosis, and gastric secretion steadily rose to 150% above control levels at 11 weeks. The remaining six dogs were allowed to develop a fatty liver for eight weeks before treatment with pancreatin and methionine was initiated. In three the liver function returned to normal, but there was no alteration of the steady rise in pouch secretion to 376% above control levels at 16 weeks. In the other three dogs the liver function did not return to normal and their average pouch secretion levels rose steadily to 296% above control levels at 16 weeks.

Comparison of the effect of several gastrin-related compounds on acid secretion in dogs

Caerulein, desulfated caerulein, the octapeptide of cholecystokinin, cholecystokinin, and pentagastrin were compared for stimulation of acid secretion from Heidenhain pouches in dogs. Pentagastrin and desulfated caerulein evoked similar maximal rates of secretion. Caerulein and octapeptide of cholecystokinin elicited similar dose-response curves and the maximal secretory rates with these two peptides were less than 50 per cent of that of pentagastrin. Cholecystokinin failed to stimulate pouch secretion over a wide range of doses. When cholecystokinin was added to an infusion of caerulein, acid secretion was inhibited. We interpret these findings as follows: (1) sulfation of tyrosyl in position 7 from the C-terminus in peptides with the active center of gastrin is the essential feature which changes these compounds from full agonists to partial agonists for gastric secretion in dogs; (2) the difference between natural cholecystokinin and the synthetic octapeptide of cholecystokinin for acid secretion probably is due to an enterogastrone other than cholecystokinin or secretin in the cholecystokinin preparation.

The effect of selective proximal vagotomy and pyloroplasty on gastric secretion and motility in the dog.

Heidenhain pouch secretion was measured and antral motility assessed by x-ray film in dogs after selective proximal vagotomy (SPV) and selective complete vagotomy, both with and without pyloroplasty. It was found that antral motility was decreased the more the denervation was moved caudally; the greater the resulting antral stasis the greater the food-stimulated Heidenhain pouch secretion. The addition of a pyloroplasty to either vagotomy group brought the foodstimulated Heidenhain pouch secretion toward normal when the vagotomy was complete and all the way to normal in the SPV group.

Ulcerogenic potential of the incompletely resected antrum

An experiment in dogs was designed to investigate the secretory effect of vagotomy and incomplete proximal antrectomy. This occurs clinically and may be a cause of stomal ulcer as well as a contributing factor to our poor results in the management of stomal ulcer. It was shown that a 1 inch rim of retained antrum in the gastric remnant resulted in a lesser reduction in pouch secretion, even when that portion of antrum was vagally denervated. The antrum-corpus junction cannot be “eye-balled” at operation, and if the surgical procedure requires identification of this point, it should be determined by objective methods. This can be done using a pH electrode that is passed like a Levin tube preoperatively and manipulated by the surgeon to locate the margin of the acid-secreting mucosa. Gastrotomy is not needed nor is stimulation with drugs. Interpretation may be impossible if a surgical stoma close to the junction has resulted in severe regurgitant gastritis.