Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The results from a short-term (28 days) treatment of patients with duodenal ulcer are reported. The average surface of the ulcers from 40.4 mm2 (initial average value) diminished to 7.3 mm2 by the 14 th day of the treatment. The graphic study of the kinetics of healing of the ulcer process revealed that in a treatment with 0.8--1.0 g Simetidin, a diminution of the ulcer by half (t/2) could be expected by the seventh day. In 16, out of the 21 treated, the ulcer epithelized by the 14th day of the treatment. In one patient a prolonged treatment of 42 days proved to be necessary to guarantee the epithelization of the ulcer. In 2/3 of treated patients, the pain complaints, the sensation of warmth and acidity disappeared by the end of the first week of the treatment. The average values of the basic and peak acid output (BAO and PAO), the N-acetyl neuramine acid output, the gastrin basic level, GOT, GPT and creatinine in serum do not change after the treatment. A significant reduction of hemoglobin concentration in the gastric juice is established after the treatment with Simetidin.
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PMID:[Results of the short-term (28 days) cimetidine treatment of duodenal ulcer]. 38 Jan 69

There is both clinical and experimental evidence for the antigastric effect of calcitonin. A study was therefore made of gastric secretion after maximum insulin stimulation, and during its inhibition by calcitonin. Evaluation of basal acid flow and the maximum acidity peak in these two tests showed that the difference between the two peaks was related to the increase in gastrin. This was not the case during inhibition. The results show that selective evaluation of gastric secretion enables selective surgical techniques to be employed in the treatment of duodenal ulcer.
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PMID:[Calcitonin inhibition of insulin-stimulated gastric secretion. A possibility of selective evaluation of gastric secretory function]. 39 72

We studied the effect of several doses of atropine on the serum gastrin and pancreatic polypeptide responses to vagal stimulation in healthy human subjects. Vagal stimulation was induced by sham feeding. To eliminate the effect of gastric acidity on gastrin release, gastric pH was held constant (pH 5) and acid secretion was measured by intragastric titration. Although a small dose of atropine (2.3 mug/kg) significantly inhibited the acid secretory response and completely abolished the pancreatic polypeptide response to sham feeding, this dose of atropine significantly enhanced the gastrin response. Higher atropine doses (7.0 and 21.0 mug/kg) had effects on gastrin and pancreatic polypeptide release which were similar to the 2.3-mug/kg dose. Atropine (0.78 and 2.3 mug/kg) without sham feeding significantly inhibited basal acid secretion and also led to significant increases in serum gastrin above basal levels. The gastrin response to sham feeding with 2.3 mug/kg atropine was significantly greater than the sum of the gastrin responses to sham feeding alone and to 2.3 mug/kg atropine alone, indicating potentiation of vagal gastrin release by atropine. We conclude: (a) Unlike vagally mediated gastric acid secretion and pancreatic polypeptide release which can be blocked by atropine, vagal gastrin release is potentiated by atropine. This observation suggests the existence of a vagal-cholinergic pathway which normally (i.e., in the absence of atropine) inhibits gastrin release. (b) Because atropine (without sham feeding) increased basal gastrin levels, it is likely that the cholinergic pathway which inhibits gastrin release is active even when the vagus nerve is not stimulated by sham feeding.
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PMID:Effect of atropine on vagal release of gastrin and pancreatic polypeptide. 42 55

A 5-year-old girl had the symptom of vomiting for four years. Gastric analysis showed elevated basal acidity unaffected by betazole stimulation. Roentgenographic examinations of the upper gastrointestinal tract showed two ulcers in the lesser curvature of the stomach. Fasting serum gastrin values were remarkably elevated and a calcium infusion test resulted in noticeable increases in serum gastrin levels. These data were consistent with the Zollinger-Ellison syndrome. In addition, the patient demonstrated such anomalies as retarded physical and mental development, kyphoscoliosis, median cleft palate, joint contracture and unusual facies due to blepharophimosis, and malformed low-set ears. These clinical features were in accord with the Marden-Walker syndrome. To our knowledge, the present case presents the first case of the combination of these two rare entities in the literature.
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PMID:Zollinger-Ellison syndrome with Marden-Walker syndrome. Association of two rare diseases in a 5-year-old girl. 46 23

To better define the pathogenetic relationship between gastric acid secretion, serum gastrin levels and acute gastroduodenal disease in burned patients, fasting serum gastrin levels were correlated with the results of a nonaugmented gastric analysis performed in 31 hemodynamically stable burned patients. Gastroduodenoscopy documented the status of the gastric and duodenal mucosa at the time of acid analysis and serum gastrin collection. Twenty-two patients had acute gastroduodenal disease. Dffuse, superficial, gastroduodenal erosions were present in 17 patients; five additional patients had ulcerative lesions. Nine patients had normal endoscopic examinations. Gastrin levels were not predictive of the incidence, severity or location of disease. Gastric acidity, however, did correlate with disease severity-correlation coefficient, r=+0.41,p less than 0.05-being lowest in normal persons, intermediate in superficial disease and highest in ulceration. There was no correlation between the levels of serum gastrin and gastric acid secretion. The relative hyperacidity in patients with acute gastroduodenal disease suggests that acid may be one of the factors potentiating mucosal injury in these patients and may be particularly important in the evolution of life-threatening ulceration.
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PMID:Gastrin levels and gastric acidity in the pathogenesis of acute gastroduodenal disease after burns. 83 63

Gastric secretion was studied in 188 fetuses of 28 pregnant dogs near term. Baseline secretory values were determined and gastric secretion was stimulated in additional fetuses with histamine, insulin, or gastrin. A significant increase in volume, acidity and pepsin output was observed in fetuses stimulated during the last week of gestation. Following maternal stimulation the placental transfer of histamine, insulin, and gastrin are demonstrated.
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PMID:[Animal-experiment studies on the pathogenesis of peptic ulcer in the newborn]. 103 12

The mechanism by which magnesium acts on gastric acid secretion is obscure. It has been demonstrated that magnesium inhibits basal as well as hypercalcemic-induced acid secretion. It has furthermore been shown that magnesium does not interfere with gastrin release. It is not, however, known if magnesium acts as an antagonist to gastrin. To elucidate this the combined effect of pentagastrin (0.5 mug/kg-hr) and magnesium sulphate (0.4 meq Mg++/kg-hr) was studied in 10 healthy subjects. The secretory plateau obtained during pentagastrin infusion was unchanged during the combined infusion of pentagastrin and magnesium. This applies to volume secretion, acidity as well as acid output.
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PMID:The combined effect of pentagastrin and magnesium on gastric acid secretion in man. 112 55

Using gastrin-like AOC-tetrapeptide the secretory function of the stomach of Japanese with endoscopically normal gastric mucosa was examined in a multicenter clinical study. Mean one hour secretion volume, mean maximal acidity, and mean maximal acid output were found to be 129.3 +/- 60.0 ml/hr, 103.7 +/- 32.4 mEq/l, and 9.2 +/- 6.9 mEq/hr respectively. Results were analysed according to sex or age by analysis of variance and compared further with the corresponding data reported in the literature.
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PMID:Secretory function of the stomach of Japanese with endoscopically normal gastric mucosa. 123 95

Mucosal secretion and blood flow of a Heidenhain pouch were measured in dogs after orally administered ethanol at doses from 0.25 to 2 g/kg of body weight. Under these conditions, the volume, free and total acidity of the gastric juice as well as mucosal blood flow increased linearly with the dose up to 1 g/kg. In all cases volume secreted and acidity chanm the other parameters and could not be correlated with blood flow. The influence of gastrin and the modification of membrane permeability are discussed with regard to these data.
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PMID:Effects of ethanol on the secretion and mucosal blood flow of a denervated gastric pouch in the dog. 123 65

The mechanisms by which administration of the H+,K(+)-ATPase inhibitor B 831-78 or intragastric perfusion with NaHCO3 induces plasma gastrin release were studied in the rat. Experiments were performed after a washout of residual intragastric contents in fasted animals provided with chronic gastric fistulae. Acute and chronic administration of B 831-78 elevated plasma gastrin dose-dependently up to 5-6 times above control levels, while the increase was only twofold with intragastric NaHCO3 infusion despite similar neutralization of gastric acidity. The profound hypergastrinaemia induced by the H+,K(+)-ATPase inhibitor, after both acute and chronic treatment, was completely prevented or reversed by intragastric perfusion with physiological amounts of acid (0.15 N HCl, 2.5 ml/h). The hypergastrinaemia was, however, largely resistant to high doses of atropine (4.3 mumol/kg) and of the M1 selective muscarinic antagonist telenzepine (10 mumol/kg). In contrast, the modest increase in plasma gastrin induced by gastric perfusion with NaHCO3 was completely suppressed by the high atropine dose and was attenuated by small doses of atropine or telenzepine (0.01 mumol/kg and 1 mumol/kg). These results demonstrate that, in the rat, blockade of the H+,K(+)-ATPase can potently induce gastrin release in the absence of a meal. Moreover, they suggest that interruption of the negative feedback between acid and gastrin release is the main mechanism through which this class of drugs releases gastrin in the rat. Since a similar degree of gastrin release cannot be achieved by alkalinization of gastric contents, additional hormonal or neural regulatory factors may contribute to the drug-induced hypergastrinaemia.
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PMID:Effect of acute and chronic acid suppression on plasma gastrin release in the rat. 131 89


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