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

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.

Effect of total adrenalectomy on gastric secretion in chronic gastric fistula rats

1964 ◽  
Vol 206 (6) ◽  
pp. 1309-1314 ◽  
Author(s):  
S. P. Bralow ◽  
S. A. Komarov ◽  
H. Shay
Keyword(s):  
Gastric Secretion ◽  
Parietal Cell ◽  
Free Acid ◽  
Acid Output ◽  
Cell Mass ◽  
Chloride Concentration ◽  
Sham Operation ◽  
Gastric Fistula ◽  
Total Acid ◽  
Total Chloride

Basal gastric secretion of rats with chronic fistulas was studied before and after adrenalectomy or sham operation. A marked exponential fall in concentration and output of free and total acid resulted in virtual anacidity within 3–7 weeks following adrenalectomy. Failure in parietal cell secretion was not accompanied by significant decrease in parietal cell mass. Pepsin concentration and output as well as volume also fell exponentially but more gradually. No significant change in total chloride concentration occurred. Relative influence of concentration in determining output was 30 times greater than volume for free acid, 3 times greater for total acid, and twice as great for pepsin. Volume was responsible for almost all variability in total chloride output. Time after adrenalectomy influenced variability of volume and acid output twice as much as concurrent decrease in body weight.

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.

Effect of thiamine deficiency on canine gastric secretion of acid

1959 ◽  
Vol 197 (2) ◽  
pp. 253-256 ◽  
Author(s):  
Marjorie K. Lavers ◽  
Patricia A. Stefanik ◽  
Charles F. Code
Keyword(s):  
Body Weight ◽  
Hydrochloric Acid ◽  
Gastric Mucosa ◽  
Gastric Secretion ◽  
Thiamine Deficiency ◽  
Acid Output ◽  
Nervous Stimulation ◽  
Deficiency State ◽  
Bethanechol Chloride ◽  
Secretory Capacity

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.

scholarly journals Effects of Parietal Cell Vagotomy on Acid and Pepsin Secretion in Gastric Fistula Dogs

1973 ◽  
Vol 178 (2) ◽  
pp. 204-208 ◽  
Author(s):  
ARI KAYNAN ◽  
CUR BEN-ARI ◽  
ALLAN E. KARK ◽  
JACK RUDICK
Keyword(s):  
Parietal Cell ◽  
Gastric Fistula ◽  
Pepsin Secretion ◽  
Parietal Cell Vagotomy

Vagotomy confined to the acid-secreting mucosa of the stomach

1987 ◽  
Vol 73 (1) ◽  
pp. 25-30
Author(s):  
E. P. Dewar ◽  
N. S. Williams ◽  
M. F. Dixon ◽  
D. Johnston
Keyword(s):  
Gastric Secretion ◽  
Myenteric Plexus ◽  
Acid Output ◽  
Gastric Wall ◽  
Neural Tissue ◽  
Gastric Fistula ◽  
Gastric Acid Output ◽  
Before And After ◽  
Acid Secreting ◽  
Gastric Musculature

AbstractChemoneurolysis, using varying concentrations of ethyl alcohol, was performed in dogs with a total gastric fistula in an attempt to denervate selectively only the acid-secreting mucosa, leaving the muscle innervated. Tests of gastric secretion and histological examination of gastric wall biopsies were performed both before and after chemoneurolysis. Chemoneurolysis resulted in a significant reduction in the number of parasympathetic fibres in the submucosa (p<0.01) and a decrease in insulin and pentagastrin stimulated acid secretion. The appearances of the myenteric plexus and gastric musculature were unchanged. The destruction of the submucosal neural tissue was, however, insufficient to produce a th erapeutically significant decrease in gastric acid output.

Effect of Atropine on Histamine-Stimulated Gastric Secretion in the Dog

1956 ◽  
Vol 186 (3) ◽  
pp. 373-376 ◽  
Author(s):  
Henry D. Janowitz ◽  
Franklin Hollander
Keyword(s):  
Gastric Secretion ◽  
Parietal Cell ◽  
Acid Output ◽  
Inhibitory Effect ◽  
Atropine Sulphate ◽  
Secreting Cell ◽  
Secretory Rate ◽  
Acid Secreting ◽  
The Mean

Inhibitory effect of atropine on gastric acid secretion was studied in four dogs with vagally denervated corpus pouches, stimulated by 0.025 mg of histamine-base subcutaneous every 10 minutes. The mean inhibition of acid output in the 3rd hour after subcutaneous injection of atropine sulphate was 29% at 0.1 mg/kg body weight, 31% at 0.2 mg/kg, and 96% at 0.4 mg/kg. At the highest dosage, inhibition was virtually complete in six of seven experiments. Since current concepts of cholinergic blocking action by atropine on gastric secretion are not completely explanatory of the present results, possible alternative formulations of the role of acetylcholine and histamine in stimulating the parietal cell are presented. One of these postulates that histamine is the final common chemical pathway for all stimuli to the acid secreting cell. The existing evidence for this is reviewed briefly. In addition, further striking evidence is presented to support the hypothesis that the primary (parietal cell) acidity is relatively constant and independent of the secretory rate.

Potassium in mecholyl-stimulated gastric secretion in the dog

1962 ◽  
Vol 202 (4) ◽  
pp. 721-724 ◽  
Author(s):  
J. Lawrence Werther ◽  
Franklin Hollander
Keyword(s):  
Gastric Secretion ◽  
Gastric Juice ◽  
Acid Output ◽  
Basic Process ◽  
Volume Rate ◽  
Concentration Time ◽  
Initial Rise ◽  
Late Fall ◽  
K Concentration ◽  
Early Rise

Previous work indicated that K concentration ([K]) of gastric juice rises abruptly after histamine injection, concomitantly with acid efflux. Using Heidenhain and vagal pouch dogs, these experiments (26 in all) were repeated with mecholyl and histamine. The concentration-time curves for K were similar for both stimuli with early rise in [K], its late fall below preinjection level, and eventual recovery. The initial rise tended to be smaller and occurred less often with mecholyl. Its occurrence after histamine was also inconsistent. [K] was poorly correlated with both acidity and volume-rate. Time curves for K output likewise were similar with both stimuli, but correlation with acid output was high. Exogenous histamine is not essential to this K efflux, which may represent a basic process associated with glandular, neural, or muscular stimulation in general.

Effect of somatostatin on basal and stimulated gastric secretion in the cod, Gadus morhua

1988 ◽  
Vol 254 (2) ◽  
pp. G183-G188 ◽  
Author(s):  
B. Holstein ◽  
C. Cederberg
Keyword(s):  
Gastric Secretion ◽  
Acid Secretion ◽  
Gastric Acid ◽  
Gadus Morhua ◽  
Acid Output ◽  
Pepsin Secretion ◽  
Basal Acid Output ◽  
Basal Acid ◽  
Slight Inhibition

In vivo secretion of gastric acid and pepsin has been studied in pylorus-ligated cod. Basal acid output amounted to 100-150 mumol H+.kg-1.h-1 and pepsin secretion to 1 mg.kg-1.h-1. In response to bombesin nonapeptide (2.4 nmol.kg-1.h-1) and histamine (81 nmol.kg-1.h-1), acid secretion increased to approximately 200 and 600% of the basal level, respectively. Pepsin output was marginally affected by histamine but increased to approximately 3 and 15 times the basal level during treatment with bombesin and eledoisin (3.27 nmol.kg-1.h-1). Somatostatin (SS-14, 15 nmol.kg-1.h-1) inhibited basal acid secretion by 85%. It also inhibited the acid secretion during stimulation with bombesin (68%) and histamine (57%), but although the former effect could be explained by removal of the basal component, the latter could not. Basal pepsin secretion was not affected by SS-14. A slight inhibition (28%) of the peak pepsin response to eledoisin was demonstrated, and bombesin failed to stimulate pepsin secretion during treatment with SS-14. These results indicate that endogenous somatostatin, if present in the cod stomach, could play a role in the regulation of gastric secretion.

Dissociated response of acid and pepsin secretion to omeprazole in an in vitro perfused mouse stomach

1984 ◽  
Vol 247 (3) ◽  
pp. G240-G247
Author(s):  
C. J. Fimmel ◽  
M. M. Berger ◽  
A. L. Blum
Keyword(s):  
Acid Secretion ◽  
Parietal Cell ◽  
Pepsin Secretion ◽  
Weak Base ◽  
Carbonyl Cyanide ◽  
Luminal Perfusion ◽  
Dose Dependent Fashion ◽  
K Concentration ◽  
Dose Dependent

The effect of omeprazole, an inhibitor of the parietal cell H+-K+-ATPase, on pepsin and acid secretion was studied in an in vitro perfused whole mouse stomach model. Omeprazole inhibited basal and dibutyryl cAMP (DBcAMP)- and histamine-stimulated acid secretion in a dose-dependent fashion with a maximally effective dose of 10(-4) M. At the same time, omeprazole induced a dose-dependent increase of unstimulated pepsin release. This increase was not affected by pretreatment with 10(-3) M atropine or 10(-4) M cimetidine. It was, however, inhibited by preincubation with 10(-4) M carbonyl cyanide m-chlorophenylhydrazone (CCCP). Pepsin secretion after maximally effective doses of histamine or DBcAMP was not affected by 10(-4) M omeprazole. In a concentration of 10(-5) M, the effect of omeprazole was additive to the effect of submaximal concentrations of carbachol and histamine. NaSCN and imidazole mimicked the effect of omeprazole on acid secretion, but pepsin release was only stimulated with 10(-2) M imidazole. Another weak base, benzylamine, stimulated acid and pepsin in parallel. Luminal perfusion with solutions of high K+ concentration did not enhance basal pepsin release. The dissociated response of acid and pepsin secretion indicates that omeprazole does not act selectively on the parietal cell. The stimulation of pepsin secretion might be related to the weak base properties of the compound.

Effect of restraint on gastric acidity in the rat

1962 ◽  
Vol 202 (4) ◽  
pp. 812-814 ◽  
Author(s):  
David A. Brodie ◽  
Richard W. Marshall ◽  
Oscar M. Moreno
Keyword(s):  
Gastric Secretion ◽  
Acid Concentration ◽  
Gastric Content ◽  
Free Acid ◽  
Acid Output ◽  
Important Change ◽  
Gastric Fistula ◽  
Total Acid ◽  
Chronic Fistula ◽  
Collection Period

Chronic gastric fistula rats were prepared by implanting stainless steel cannulas in the rumen portion of the stomachs of male Holtzman rats and gastric content was collected in both the unrestrained and restrained state. Gastric secretion in acute pylorus-ligated rats, unrestrained and restrained, was studied at the same time. Volume of gastric content, free and total acidity, and free acid output were significantly lower in the chronic fistula rats as compared to the pylorus-ligated rats in the initial 4-hr collection period. A study of 24-hr gastric content in chronic fistula rats showed that restraint produced a significant decrease in volume, a significant increase in free and total acid concentration, and no change in free acid output, while the restrained pylorus-ligated rats had a significant decrease in volume, no change in free or total acid concentration, and a significant decrease in free acid output as compared with control values. This suggests that an increase in acid concentration is an important change produced in gastric secretion by restraint stress.

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