Effect of cimetidine on histamine-stimulated gastric acid and electrolytes in dogs

1983 ◽  
Vol 244 (4) ◽  
pp. G416-G420
Author(s):  
B. I. Hirschowitz ◽  
E. Molina
Keyword(s):  
Acid Secretion ◽  
Gastric Acid ◽  
Gastric Juice ◽  
Gastric Volume ◽  
Histamine Stimulation ◽  
H2 Receptor ◽  
High Doses ◽  
Volume Output ◽  
Induced Changes ◽  
Histamine Binding

Intravenous administration of cimetidine (0.25-2.0 mg X kg-1 X h-1) inhibited histamine-stimulated gastric acid secretion in both intact (Ki = 1.0 mg X kg-1 X h-1) and vagotomized (Ki = 1.75 mg X kg-1 X h-1) dogs. During histamine infusion, all doses of cimetidine reduced gastric volume output; high doses increased gastric juice pepsin and [Na+] and reduced [H+] and [Cl-]. Gastric juice [K+] was not affected during cimetidine infusion. The cimetidine-induced changes in electrolyte concentrations were qualitatively comparable with those observed on withdrawal of histamine stimulation. On termination of cimetidine infusion with continued histamine administration, gastric [K+] and volume output increased immediately, followed 30 min later by an increase in [H+] and a reciprocal decrease in [Na+]; [Cl-] did not recover. The changes in gastric juice electrolytes after termination of cimetidine, with the exception of [Cl-], mimicked the changes observed on initiation of histamine stimulation. These data indicate that the effects of cimetidine may be totally explained by its antagonism of histamine binding to the parietal cell H2-receptor, that vagotomy reduces cimetidine binding to the H2-receptor, and that cimetidine antagonism of histamine is rapidly reversed on removal of the antagonist.

Effects of tachykinins on gastric acid and pepsin secretion and on gastric outflow in the Atlantic cod, Gadus morhua

1986 ◽  
Vol 250 (3) ◽  
pp. G309-G315 ◽  
Author(s):  
B. Holstein ◽  
C. Cederberg
Keyword(s):  
Substance P ◽  
Acid Secretion ◽  
Gastric Acid ◽  
Gadus Morhua ◽  
Atlantic Cod ◽  
Gastric Volume ◽  
Pepsin Secretion ◽  
Secretory Rate ◽  
Related Peptide ◽  
High Doses

Gastric acid and pepsin responses to substance P, physalaemin, eledoisin, and an eledoisin-related peptide, [Lys6]eledoisin-(6-11), were measured in gastrically and intestinally perfused cods. The intestinal perfusion maintains water balance and inhibits drinking. During basal conditions acid secretion was stimulated (approximately equal to 25%) by low doses (less than 0.13 nmol X kg-1 X h-1) of physalaemin and eledoisin. High doses (greater than 16 nmol X kg-1 X h-1) were inhibitory. Median and very high doses of substance P and eledoisin-related peptide, respectively, tended to stimulate acid secretion. All tachykinins were extremely efficacious pepsigogues. Physalaemin and eledoisin were the most potent (D50 approximately 10(-10) mol X kg-1 X h-1) but produced fading and submaximal responses at high doses. The fading persisted despite endogenous acidification produced by histamine stimulation. Relative to physalaemin, the potencies of substance P and eledoisin-related peptide were 0.04 and 0.001. The results suggest that some tachykinin may be a physiological stimulator of pepsin secretion and that the effect on acid secretion results from activation of both stimulatory and inhibitory pathways. The inhibitory component probably includes a cholinergic link. Gastric volume outflow increased during infusion of physalaemin, eledoisin, and (slightly) substance P. The response, which was not related to acid secretory rate (and conceivably not to volume secretion), suggests that a tachykinin may be involved also in the regulation of drinking.

A model study of the regulation of gastric acid secretion

1989 ◽  
Vol 257 (1) ◽  
pp. G157-G168 ◽  
Author(s):  
B. Van Duijn ◽  
D. L. Ypey ◽  
J. de Goede ◽  
A. A. Verveen ◽  
W. Hekkens
Keyword(s):  
Duodenal Ulcer ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Gastric Volume ◽  
Gastric Ph ◽  
Food Storage ◽  
Computer Simulation Model ◽  
Gastrin Secretion ◽  
Ph Dependent

A computer simulation model is presented of the gastric phase regulation of gastric acid secretion in humans. The model is based on experimental data from the literature and includes terms representing gastric pH and gastric volume-dependent gastrin secretion, gastrin-dependent acid secretion, food storage in the stomach, and gastric emptying. We have explored the predictive value of the model in assessing the relative importance of gastric pH-dependent and gastric volume-dependent acid secretion mechanisms under various conditions. Similarly we have studied the role of gastric acid deregulation in achlorhydria, the Zollinger-Ellison syndrome, and duodenal ulcer, and the influence of the antacid drugs cimetidine and ranitidine under duodenal ulcer conditions. Model analysis of normal gastric acid regulation suggests that gastric volume-controlled acid secretion is of major importance during eating and predicts that pH-dependent gastrin secretion is of major importance in preventing excessively low pH levels between meals and during the night.

Ventromedial hypothalamic lesions elevate basal and cephalic phase gastric acid output

1980 ◽  
Vol 239 (3) ◽  
pp. G221-G229 ◽  
Author(s):  
H. P. Weingarten ◽  
T. L. Powley
Keyword(s):  
Weight Gain ◽  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Acid Output ◽  
Gastric Acid Output ◽  
Full Development ◽  
Cephalic Phase ◽  
A New Technique ◽  
Induced Changes

With the use of a new technique for the measurement of gastric acid output in the rat, this study identifies ventromedial hypothalamic (VMH) lesion-induced changes in gastric acid secretion. Basal and cephalic phase gastric acid secretion were monitored in VMH- and sham-lesioned control rats on days 1, 5, 9, 13, and 17 postlesion as well as after the full development of obesity. VMH lesions resulted in increases of both phases of secretion. The magnitude of hypersecretion in lesioned rats developed with time and was fully developed by day 9 postlesion. The hypersecretion did not require a hyperphagia or weight gain, but its degree correlated with subsequent weight gain. These data, in conjunction with a review of VMH lesion effects on insulin secretion, suggest a widespread effect of VMH lesions on visceral secretory responses. The relevance of these data to the etiology of the VMH syndrome is discussed.

Tubeless tests for gastric acid

1964 ◽  
Vol 2 (23) ◽  
pp. 91-92
Keyword(s):  
Acid Secretion ◽  
Gastric Acid Secretion ◽  
Gastric Acid ◽  
Gastric Juice ◽  
False Negative ◽  
Pernicious Anaemia ◽  
Rheumatoid Disease ◽  
Negative Results ◽  
False Negative Results ◽  
Hypochromic Anaemia

Absence of gastric acid secretion (anacidity, pH of gastric juice 7 or over) or abnormally low gastric acid secretion (achlorhydria, pH of gastric juice between 3. 6 and 7, depending on the definition) is evidence of the atrophy of gastric mucosa which is always present in adults with pernicious anaemia, and often accompanies chronic hypochromic anaemia, rheumatoid disease, myxoedema, diabetes mellitus, aplastic anaemia, steatorrhoea, and gastric carcinoma; it also occurs in relatives of patients with pernicious anaemia. The only indication for the use of tubeless tests is to demonstrate gastric acid secretion, thus excluding the diagnosis of pernicious anaemia in an anaemic adult. The tests can reliably show that acid is present, but they cannot show conclusively that acid is absent: false negative results are not uncommon. 1–3 For this reason some consultants doubt whether these tests are worth using.

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