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Results for “HYDROCHLORIC ACID”

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At least 721 records · Page 40Linked to original sources
PubMed1977

Inhibition of hydrochloric acid and pepsin secretion from gastric pouches by antral pouch acidification in sheep.

1. Secretion of acid and pepsin from separated pouches of the body of the abomasum was studied in sheep during perfusion of antral pouches with acid solutions. 2. Resting secretion of acid and pepsin was reduced by acidification of antral pouches to pH 2.7 or less. 3. Increases in the secretion of HCl and pepsin normally obtained on feeding were reduced or abolished by perfusion of antral pouches with solutions at pH 1.3--2.0. 4. Perfusion of antral pouches with acetylcholine at pH 2.5 failed to stimulate acid secretion as it did at a higher pH. 5. Pentagastrin stimulated acid and pepsin secretion during the inhibition of secretion produced by antral pouch acidification. 6. Increases in reticular motility occurred on antral pouch acidification with solutions of pH 1.1--1.3. 7. The contribution of antral pH in regulating abomasal acid secretion is discussed.

Abomasum↗
PubMed1978

Secretion of intrinsic factor and hydrochloric acid after 12 weeks' treatment with cimetidine.

A sample of 16 patients had pentagastrin stimulation studies performed before starting a 12 week course of cimetidine, and again 12 hours after completing the course. Basal and pentagastrin stimulated intrinsic factor secretion was assayed in 13 patients. There was no significant difference in the pattern of secretion after 12 weeks' treatment with cimetidine. The basal and peak acid outputs of all 16 patients were measured. No significant difference was found in the pattern of acid secretion after treatment. It appears that parietal cell secretory function is restored to normal within 12 hours of discontinuing a prolonged course of cimetidine.

Cimetidine↗
PubMed1986

Amelioration of hypoxia-induced lactic acidosis by superimposed hypercapnea or hydrochloric acid infusion.

Recent studies have shown that ketoacid production is exquisitely sensitive to changes in systemic pH, with a decrease inhibiting and an increase stimulating the production rate. To determine whether inhibition of net endogenous acid production is a widely applicable mechanism for the defense of acid-base homeostasis, we examined the effect of superimposed acidosis on lactic acid production by hypoxic rats. Anesthetized paralyzed mechanically ventilated rats with normocapnia increased blood lactate progressively in response to a fractional inspired O2 (FIO2) of 8% (PaO2, 35-38 mmHg) and achieved a level of 7.0 +/- 1.2 mM at 3 h. Superimposition of either mild respiratory acidosis (PCO2, 59 mmHg) or exogenous inorganic metabolic acidosis (intra-arterial HCl sufficient to decrease pH from 7.33 to 7.23) after 1 h of hypoxia dramatically diminished the rise in blood lactate. At the end of the third hour, blood lactate levels averaged 1.7 +/- 0.6 mM with superimposed respiratory acidosis and 2.7 +/- 0.4 mM with superimposed metabolic acidosis, both values being significantly less than the hypoxic controls. Termination of the superimposed respiratory acidosis resulted in a rapid increase in blood lactate levels, demonstrating the reversibility of the pH modulation of lactic acid production. Thus systemic acidosis appears to feed back in a protective fashion to inhibit net lactic acid production in rats with hypoxia-induced lactic acidosis. These findings suggest that finely tuned feedback control mechanisms that keep systemic pH within a narrow range operate under both major conditions of enhanced endogenous acid production (i.e., keto- and lactic acidosis).

Acidosis↗
PubMed1978

Hydrochloric acid and cyclic 3'.5'-adenosine monophosphate content of rodent gastric juice after halothane administration.

Pulmonary aspiration of gastric contents during general anesthesia has always been a serious problem. Morbidity and mortality depend on the volume and acidity of the aspirated material. The anesthetic agent itself might affect gastric acid secretion. The effect of halothane (5, 10 and 20 mg/kg intravenously) on HCl secretion and cAMP content of gastric juice in pyloric and cardiac ligated male Sprague-Dawley rats was investigated. Compared with the control group, halothane significantly increased both HCl secretion and cAMP content of gastric juice, but to a lesser degree at the higher doses (p less than 0.05).

Animals↗
PubMed1975

The influences of propranolol on serum gastrin concentration and hydrochloric acid secretion in response to hypoglycemia in normal subjects.

In ten normal subjects the effect of propranolol on serum gastrin concentration and HC1 secretion during insulin hypoglycemia (0.2 U/kg) was studied. Under the influence of propranolol (50 mug/kg intravenously in 3 min) the gastrin response to insulin was abolished. The insulin-induced HC1 secretion was reduced by propranolol from 38 to 18 mEq/2h (p less than 0.01). These results are compatible with the hypothesis of beta-adrenergic stimulation on serum gastrin concentration and HC1 secretion during insulin hypoglycemia.

Adolescent↗
PubMed1975

Secretion of hydrochloric acid in Ghosh-Lai rat preparation following stimulation with histamine and pentagastrin and inhibition by gastrone and atropine.

In this study of 48 successfully operated rats, we evaluated the applicability of the Ghosh-Lai stomach preparation to the quantitation of the HCl output following stimulation with histamine and pentagastrin and inhibition with gastrone and atropine. The usefulness of this rat preparation was well demonstrated and good duplication of results was obtained with various doses of histamine and pentagastrin. In this rat preparation, the HCl output following an optimal pentagastrin dose of 6 mug/kg/30 min i.v. was almost twice higher than that after an optimal histamine dose - for this rat preparation - of 0.2 mg/kg/30 min i.v. The inhibitory effect of gastrone B on histamine-stimulated HCl output has been confirmed in this rat preparation and shown to extend also on the pentagastrin-stimulated HCl secretion. The comparison of the atropine and gastrone inhibition of the pentagastrin-stimulated HCl output in the Ghosh-Lai preparation indicates that the inhibitory effect of 40 mug gastrone i.v. is similar in rat to that of 0.4 mg atropine sulfate i.v. under these conditions.

Animals↗
PubMed1975

Formaldehyde-hydrochloric acid treatment. A fluorescence histochemical method for the demonstration of tryptophan residues in peptides and proteins.

Treatment with formaldehyde gas and HCl vapor, simultaneously or in sequence, induces fluorescence with indoles, including tryptophan residues of peptides, as is evident from studies on protein droplet models. Among cells that display intense formaldehyde-HCl-induced fluorescence are pancreatic exocrine cells, gastric chief cells, Paneth cells and enterochromaffin cells. Peptide hormone-producing cells that can be visualized by the formaldehyde-HCl treatment include gastrin cells and glucagon cells. The simultaneous procedure has proved superior to the sequential procedure. Simultaneous formaldehyde-HCl treatment appears to be a useful method for the demonstration of tryptophan residues of peptides and proteins. It seems more sensitive than previously described indole methods.

Animals↗