Effect of thiamine deficiency on canine gastric secretion of acid

A study was undertaken to determine the effect of thiamine deficiency on the hydrochloric acid output of vagally denervated gastric pouches (Heidenhain-type) and vagally innervated gastric pouches (Pavlov-type) in dogs. Responses of both types of pouches to injection of 0.05 mg of histamine/kg of body weight and the maximal secretory capacity of both types after histamine were unaltered during the deficiency state. A degree of thiamine deficiency sufficient to produce anorexia and neuritis was without effect on the secretory response of canine gastric mucosa to histamine. The hydrochloric acid output of vagally innervated pouches during nervous stimulation caused by insulin-induced hypoglycemia was drastically reduced as soon as thiamine deficiency developed, while the response to bethanechol chloride was little, if at all, affected. It is concluded that the vagal secretory mechanism participates in the general neural failure of thiamine deficiency and that this failure most likely is in the neurons of the vagal nuclei.

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The development of acid and pepsin (EC 3. 4. 23. 1) secretory capacity in the pig; the effects of age and weaning

British Journal Of Nutrition ◽

10.1079/bjn19850113 ◽

1985 ◽

Vol 54 (1) ◽

pp. 305-320 ◽

Cited By ~ 28

Author(s):

Peter D. Cranwell

Keyword(s):

Body Weight ◽

Hydrochloric Acid ◽

Acid Output ◽

Regression Line ◽

Solid Food ◽

Large White ◽

Protein Nitrogen ◽

Positive Correlations ◽

Stomach Weight ◽

Secretory Capacity

1. The development of gastric secretory capacity of hydrochloric acid and pepsin (EC 3. 4. 23. 1) was studied in thirty-eight Large White x Landrace pigs from the litters of six sows (three pairs of two), 9–38 d of age. The pigs of each pair of sows were born within 24 h of each other. The pigs of a litter were paired according to sex and size and cross-fostered, i.e. one pig from each pair was allocated to each sow.2. One litter from each pair was reared entirely by the sow (milk-fed, MF) whereas the other litter was reared by the sow for 21 d, but was allowed access to solid food (210 g crude protein (nitrogen x 6.25)/kg) at 12 d and was entirely dependent on solid food after 21 d (creep-fed, CF).3. Following a 14–18 h fast, pigs were anaesthetized (Halothane–sodium pentobarbitone) and their stomachs perfused a a constant rate with Ringer solution. Gastric secretion was stimulated by intravenous infusion of betazole hydrochloride (Histalog) at 3 mg/kg per h for 2 h. Hydrochloric acid and pepsin were measured in the perfusate which was collected at 15-min intervals.4. There were significant positive correlations between stomach weight and body-weight for both MF and CF pigs. The slope of the regression line for CF pigs was significantly greater than that for MF pigs (P < 0.01).5. There were significant positive correlations between maximal acid output and stomach weight for both MF and CF pigs.6. There were significant positive correlations between maximal pepsin output and stomach weight for both MF and CF pigs. The slope of the regression line for CF pigs was significantly different from that for MF pigs (P < 0.01). There were also significant positive correlations between maximal pepsin output per unit stomach weight and stomach weight for both MF and CF pigs.7. The pattern of development of pepsin secretory capacity in both CF and MF pigs was different from that for acid secretion. Maximal outputs of acid per unit stomach weight for MF and CF pigs remained relatively constant. Maximal outputs of pepsin per unit stomach weight and per unit body-weight increased with age for both MF and CF pigs.8. The results indicate that pigs given access to solid food before weaning and weaned on to solid food have heavier stomachs and greater acid and pepsin secretory capacity than pigs fed entirely on sows' milk.

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Inhibition of cephalic and antral phases of gastric secretion by antral chalone

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1962.202.4.716 ◽

1962 ◽

Vol 202 (4) ◽

pp. 716-720 ◽

Cited By ~ 16

Author(s):

James C. Thompson ◽

Harvey J. Lerner ◽

Jorge A. Tramontana

Keyword(s):

Hydrochloric Acid ◽

Gastric Secretion ◽

Portal Vein ◽

Acid Secretion ◽

Acid Output ◽

Insulin Hypoglycemia ◽

Heidenhain Pouch ◽

Pavlov Pouch

The effect of antral acidification on the antral and cephalic phases of gastric secretion has been studied. Cross-transfusions were carried out between pairs of dogs in which blood from the portal vein of one dog was administered to another dog with a denervated fundic pouch. Transfusion of blood collected during acidification of the antrum resulted in a diminution of Heidenhain pouch acid secretion in response to food and to topical acetylcholine of 64% and 83%, respectively. The effect of antral acidification on gastric secretion stimulated by insulin hypoglycemia was studied in dogs prepared with Pavlov and isolated antral pouches (innervated and denervated). Irrigation of the antral pouch with .1 n hydrochloric acid resulted in a 92% decrease in Pavlov pouch acid output.

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Role of Na-K-2Cl cotransporter-1 in gastric secretion of nonacidic fluid and pepsinogen

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00095.2005 ◽

2005 ◽

Vol 289 (3) ◽

pp. G550-G560 ◽

Cited By ~ 28

Author(s):

Nichole McDaniel ◽

Amy J. Pace ◽

Stefanie Spiegel ◽

Regina Engelhardt ◽

Beverly H. Koller ◽

...

Keyword(s):

Gastric Mucosa ◽

Gastric Secretion ◽

Acid Secretion ◽

Acid Output ◽

Gastric Gland ◽

Electrical Current ◽

Fluid Secretion ◽

Parietal Cells ◽

Pepsinogen Secretion ◽

Deficient Mice

Na-K-2Cl cotransporter-1 (NKCC) has been detected at exceptionally high levels in the gastric mucosa of several species, prompting speculation that it plays important roles in gastric secretion. To investigate this possibility, we 1) immunolocalized NKCC protein in the mouse gastric mucosa, 2) compared the volume and composition of gastric fluid from NKCC-deficient mice and their normal littermates, and 3) measured acid secretion and electrogenic ion transport by chambered mouse gastric mucosa. NKCC was localized to the basolateral margin of parietal cells, mucous neck cells, and antral base cells. In NKCC-deficient mice, gastric secretions of Na+, K+, Cl−, fluid, and pepsinogen were markedly impaired, whereas secretion of acid was normal. After stimulation with forskolin or 8-bromo-cAMP, chambered corpus mucosa vigorously secreted acid, and this was accompanied by an increase in transmucosal electrical current. Inhibition of NKCC with bumetanide reduced current to resting levels but had no effect on acid output. Although prominent pathways for basolateral Cl− uptake (NKCC) and apical Cl− exit [cystic fibrosis transmembrane conductance regulator (CFTR)] were found in antral base cells, no impairment in gastric secretion was detected in CFTR-deficient mice. Our results establish that NKCC contributes importantly to secretions of Na+, K+, Cl−, fluid, and pepsinogen by the gastric mucosa through a process that is electrogenic in character and independent of acid secretion. The probable source of the NKCC-dependent nonacidic electrogenic fluid secretion is the parietal cell. The observed dependence of pepsinogen secretion on NKCC supports the concept that a nonacidic secretory stream elaborated from parietal cells facilitates flushing of the proenzyme from the gastric gland lumen.

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

Parasitology ◽

10.1017/s0031182000058418 ◽

1976 ◽

Vol 72 (1) ◽

pp. 01-12 ◽

Cited By ~ 4

Author(s):

N. Anderson ◽

R. Blake ◽

D. A. Titchen

Keyword(s):

Food Intake ◽

Gastric Secretion ◽

Acid Output ◽

Infected Sheep ◽

Total Acid ◽

Transient Period ◽

Repeated Infections ◽

Secretory Capacity ◽

Histamine Antagonist

Sheep which had been either previously infected with O. circumcincta or maintained worm-free, were surgically prepared with separated fundic pouches and abomasal cannulae and subsequently infected with 20000 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 μg.kg−1), the histamine antagonist (burimamide 8mg.kg−1) and atropine (100 μg 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.

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Effects of KCl and insulin on benzimidazole-inhibited canine gastric secretion

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1983.245.6.g739 ◽

1983 ◽

Vol 245 (6) ◽

pp. G739-G744

Author(s):

B. I. Hirschowitz ◽

J. Fong

Keyword(s):

Gastric Secretion ◽

Parietal Cell ◽

Acid Output ◽

Gastric Fistula ◽

Large Decrease ◽

Pepsin Secretion ◽

K Secretion ◽

Inhibited Acid ◽

K Concentration ◽

Bethanechol Chloride

The final step in acid secretion is believed to result from the H+-K+-ATPase-mediated exchange of H+ in the parietal cell, with K+ in the lumen. To study the K+ secretion we used Picoprazole and insulin separately and together to inhibit gastric secretion stimulated in gastric fistula dogs with histamine (100 micrograms X kg-1 X h-1). Picoprazole, a substituted benzimidazole (750 mg/kg), reduced gastric H+ concentration and volume with a rise in K+ concentration [( K+]) to 20–25 meq/l. Insulin alone inhibited acid output to the same extent as Picoprazole but with a marked fall in [K+]. Insulin (0.6 U/kg) given with Picoprazole did not alter inhibition of H+ but prevented the large decrease in gastric juice [K+]. An injection of KCl (1 meq/kg) 1 h after Picoprazole did not alter the effects of the inhibitor. Pepsin secretion after insulin was delayed by Picoprazole, whereas during bethanechol chloride infusion (80 micrograms X kg-1 X h-1) pepsin output was reduced for a shorter period and to a lesser extent than acid. We concluded that insulin affects gastric H+ and K+ secretion by a mechanism not related to H+-K+-ATPase and that Picoprazole affects pepsin secretion probably indirectly via its effect on the parietal cell, where its action is quite consistent with an effect limited to inhibition of the H+-K+-ATPase of the parietal cell.

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

Parasitology ◽

10.1017/s0031182000043134 ◽

1976 ◽

Vol 72 (1) ◽

pp. 01-12 ◽

Cited By ~ 32

Author(s):

N. Anderson ◽

R. Blake ◽

D. A. Titchen

Keyword(s):

Food Intake ◽

Gastric Secretion ◽

Acid Output ◽

Infected Sheep ◽

Total Acid ◽

Transient Period ◽

Repeated Infections ◽

Secretory Capacity ◽

Histamine Antagonist

SummarySheep which had been either previously infected with O. circumcincta or maintained worm-free, were surgically prepared with separated fundic pouches and abomasal cannulae and subsequently infected with 20000 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 μg.kg−1), the histamine antagonist (burimamide 8mg.kg−1) and atropine (100 μg 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.

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Effects of Metiamide on the Human Stomach

Clinical Science ◽

10.1042/cs0490445 ◽

1975 ◽

Vol 49 (5) ◽

pp. 445-458

Author(s):

B. Thjodleifsson ◽

K. G. Wormsley

Keyword(s):

Hydrochloric Acid ◽

Gastric Mucosa ◽

Gastric Secretion ◽

Acid Solution ◽

Barrier Function ◽

Gastric Acidity ◽

Human Stomach ◽

Secretory Response ◽

Gastric Lumen

1. The effect of metiamide on gastric acidity in man has been studied. Solutions of hydrochloric acid or glucose were instilled into the stomach and the subsequent rates of gastric secretion and emptying, and the disappearance of acid within the stomach, were measured. 2. Metiamide inhibited the gastric secretory response to the instilled acid and glucose solutions but did not change the overall pattern of emptying of the instilled solutions. 3. During administration of metiamide, there was a net loss of acid from within the gastric lumen. The rate of disappearance of acid from the instilled acid solution was small and not sufficient in magnitude to account for the metiamide-evoked decrease in the concentration of acid secreted in response to pentagastrin. 4. We conclude that metiamide does not inhibit gastric secretion by altering the ‘barrier’ function of the gastric mucosa.

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Single and repeated testing of growth hormone secretory capacity in hypopituitarism using growth hormone releasing factor

Acta Endocrinologica ◽

10.1530/acta.0.112s118 ◽

1986 ◽

Vol 113 (4_Suppl) ◽

pp. S118-S122 ◽

Cited By ~ 3

Author(s):

O. BUTENANDT ◽

M. EMMLINGER ◽

H. DOERR

Keyword(s):

Growth Hormone ◽

Body Weight ◽

Pituitary Gland ◽

Bolus Injection ◽

Hormone Deficiency ◽

Test Results ◽

Repeated Testing ◽

Plasma Growth Hormone ◽

Once Daily ◽

Secretory Capacity

Abstract 38 patients with proven growth hormone deficiency (GHD) and 19 children with familial short stature received an iv GRF-bolus injection of 1 ug/kg body weight. Whereas in all control children plasma growth hormone rose significantly (mean of maximal values 36 ng/ml), only 7 out of 38 patients with GHD reached peak values of 8 ng/ml or more. GRF-priming by 1 ug GRF/kg BW given once daily s.c. for 5 days in 19 patients improved the response of the pituitary gland in 11. Thus, following the first GRF test, only 21 % of patients demonstrated function of the pituitary gland whereas 45 % did so when all test results are combined. To evaluate the pituitary function in patients with GHD correctly, GRF tests following a GRF priming period seems to be necessary to reactivate atrophic somatotropic cells of the pituitary gland.

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