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)

In dogs, the effect of atropine on gastric acid secretion induced by food, mechanical stimuli, and histamine involved a complete block of the acid secretion but left the gastric secretory effect of histamine unaffected. Atropine caused about a twofold increase in duration of histamine-evoked acid secretion and a rise of the intragastric acidity in all parts of the stomach.
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PMID:[The effect of atropine on acid formation in the stomach]. 0 46

Cimetidine markedly inhibits gastric acid secretion, but from the therapeutic point of view it is important to know whether concurrent treatment with an anticholinergic increases its effect. This possibility has been investigated by measuring the 24 h intragastric acidity and nocturnal output of acid in four duodenal ulcer patients, each receiving on separate occasions cimetidine 1 g/day and placebo, atropine 2-4 mg/day and placebo, cimetidine and atropine, or two placebos. Cimetidine alone decreased mean hourly hydrogen ion activity by 63% of control values, decreased mean hourly hydrogen ion concentration (total acid) by 41%, inhibited nocturnal acid secretion by 83% and resulted in half the nocturnal samples being anacidic. Atropine alone had no effect when compared with control and combined treatment with both drugs was not superior to cimetidine alone. Atropine did not affect the absorption or urinary excretion of cimetidine. Fasting serum gastrin concentrations were not changed by any of the treatments. At the doses studied, the combination of cimetidine with an anticholinergic appears to offer no advantages over treatment with the H2-antagonist alone. Cimetidine is the only potent anti-secretory drug that does not cause acute side-effects and this important advantage would be lost if it were given with a maximal dose of an anticholinergic.
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PMID:24-hour intragastric acidity and nocturnal acid secretion in patients with duodenal ulcer during oral administration of cimetidine and atropine. 32 18

The inhibitory effect of 15(R)15 methyl prostaglandin E2 (Me PGE2) on the gastric acid response to pentagastrin stimulation, 0.6 micrograms.kg-1.h-1, was examined in healthy male volunteers. Each subject underwent a control test and tests with intragastrically administered graded doses of 15(R)15 Me PGE2 as free acid (80, 140, 200, and 400 micrograms, n = 5) and as methylester (80, 140, and 200 micrograms, n = 6). The percentage inhibition of the acid output during 2 h after increasing doses of the free acid was 24 +/- 11, 49 +/- 7, 44+/-9, and 76 +/- 12%. Corresponding figures for the methylester were 35 +/- 2, 54 +/- 5, and 64 +/- 8%. Both volume and acidity were reduced. Side effects did not occur, except for moderate diarrhoea in one subject after 400 micrograms of the free acid. In a third series (n = 6) the combined effect of 80 micrograms methyl ester (44 +/- 5% inhibition) and 1.5 mg atropine sulphate was studied. Atropine alone gave a 43 +/- 6% inhibition by lowering the secreted volumes. For the combination the inhibition was 82 +/- 3%. Intragastric 15(R)15 Me PGE2 inhibited dose-dependently the pentagastrin-stimulated gastric acid response. Differences between the free acid and methyl ester of the analogue were not significant. Compared with other Me PGE2 compounds, 15(R)15 Me PGE2 was less effective per dose, but the dose range was broader and side effects were slight. Concomitantly given atropine had a significant additive inhibitory effect.
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PMID:The inhibitory effect of 15(R)15 methyl prostaglandin E2 and the interaction with atropine on stimulated gastric acid secretion in man. 37 76

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

The effects of parenteral pilocarpine, atropine, and norepinephrine on salt and water transport were studied in jejunum and ileum of anesthetized rats. Pilocarpine increased jejunal transmural PD, reduced absorption of Na, K, HCO3, and H2O, and increased secretion of Cl; in ileum, it caused secretion of Na and H2O, elicited secretion of K, and reduced the absorption of Cl. In both segments, perfusate became more akaline, and there was less of a rise in PCO2. Atropine prevented all changes caused by pilocarpine. Atropine alone increased jejunal absorption of Na and HCO3 and acidity of perfusate, implying that cholinergic nerves influence transport. Norepinephrine augmented jejunal absorption of Na, Cl, and H2O but caused no change in PD. In ileum, norepinephrine increased absorption of Na and Cl, reduced the rise in pH, increased the rise in PCO2 of perfusate, but did not affect net HCO3 movement. With all agents, when Na absorption increased, perfusate became more acidic in jejunum and less alkaline in ileum, evidence of an association between Na and H transport.
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PMID:Intestinal ion transport: effect of norepinephrine, pilocarpine, and atropine. 96 67

The effects of pirenzepine on blood pressure, heart rate and gastric juice volume as well as pH were evaluated and compared with those after atropine and cimetidine in 54 adult patients divided into five groups. Patients in Groups A, P, AP, AC and ACP received atropine, pirenzepine, atropine plus pirenzepine, atropine plus cimetidine, or atropine, cimetidine plus pirenzepine, respectively. Atropine 0.5 mg and cimetidine 200 mg were given intramuscularly 60 min before induction of anesthesia, and pirenzepine 10 mg was given intravenously 5 min before induction. Gastric juice was aspirated just after, 60 and 120 min after induction of anesthesia. Mean blood pressure and heart rate remained unchanged following intravenous pirenzepine in Group P, whereas heart rate increased significantly in Groups AP and ACP. There were no significant differences in mean volume and pH of gastric juice among the groups just after and 120 min after induction of anesthesia, although gastric volume in Group AC was significantly less than in Groups P, AP and ACP 60 min after induction. Gastric pH increased gradually and gastric volume decreased slightly following intravenous pirenzepine. The incidence of samples with a pH higher than 2.5 was greater in Group AC than in Group P just after and 60 min after induction, whereas there was no difference between the two groups after 120 min. We conclude that intravenous pirenzepine 10 mg is effective to reduce gastric juice volume and acidity, and it should be given at least 60 min before induction of anesthesia.
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PMID:[Effect of intravenous pirenzepine on hemodynamics and gastric juice volume as well as pH in surgical patients]. 143 29

Gastric ulcerations induced in rats by a combination of indomethacin and cold-stress (5 +/- 1 degrees C) for 6 hr were more severe than those induced by indomethacin or cold-stress alone. The acidity of gastric juice was increased in rats treated with indomethacin plus cold-stressed. Histamine H2 receptor antagonists, (H+-K+) ATPase inhibitors and prostaglandins inhibited gastric ulcer formation in indomethacin plus cold-stress treated rats, whereas anticholinergics aggravated the ulceration. The indomethacin plus cold-stress induced acid secretion was inhibited by cimetidine and omeprazole in pylorus-ligated rats. Atropine had less effect on the increase in acidity than cimetidine and omeprazole. These findings indicate that the ulcer formation in indomethacin plus cold-stress treated rats is related the increased in acidity of gastric juice. This gastric ulcer model may be useful for evaluating antiulcer agents.
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PMID:Effects of indomethacin and cold-stress on gastric acid secretion and ulceration. The effects of anti-acid secretory agents in rats. 367 83

Sham feeding (SF) was used to evaluate the effect of physiological vagal stimulation on gastric acid (H+) and bicarbonate (HCO3-) secretion in humans, as well as on parietal and nonparietal volume secretion. A recently validated method, derived from a two-component model of gastric secretion, was employed. SF increased both H+ secretion from parietal cells (P less than 0.001) and HCO3- secretion from nonparietal cells (P less than 0.01), although the H+ response was greater and more prolonged. Atropine significantly inhibited not only H+ secretion but also HCO3- and nonparietal volume secretion. Peak H+ secretion during SF averaged approximately 27 mmol/h, whereas peak HCO3- secretion averaged approximately 6 mmol/h. When H+ secretion was already maximally stimulated by an intravenous pentagastrin infusion, SF actually reduced gastric juice acidity and osmolality due to neutralization of H+ by HCO3- and to dilution of H+ by nonparietal secretions. These studies therefore indicate that vagal stimulation induced by SF increases both H+ and HCO3- secretion in humans and that this process is cholinergically dependent.
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PMID:Gastric H+ and HCO3- secretion in response to sham feeding in humans. 397 Jan 99

Cimetidine, SKF 92334, 1-Cyano 2-methyl -3-2 (Methylimidazole -4- ylmethylthio) ethyl guanidine, C10 H16 N6 S, a competitive antagonist of H2 histamine receptors was given as a single dose orally before induction of anaesthesia in elective and emergency surgery. The volume and pH of the gastric juice were measured in 260 patients of either sex. Cimetidine was given at different times between 0 and 6 hours and was compared with control Group A who received I.M. injection of diazepam 10 mg. and atropine sulphate 0.6 mg, and control Group B who received oral diazepam 10 mg. 1-11/2 hours preoperatively. Cimetidine had maximum effect in reducing the acidity of the gastric secretion when given 2-4 hours preoperatively. Atropine had no substantial effect in reducing the pH and volume of gastric juice when administered with cimetidine.
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PMID:The preoperative use of cimetidine in reducing acidity of gastric secretion. 746 65