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 effect of H2-receptor blockade on intragastric acidity was studied in nine normal males. The pH of their gastric contents was measured at hourly daytime and two hourly nighttime intervals for 48 hours. The subjects ate identical meals, drank identical volumes of fluid, and smoked the same number of cigarettes during the two study days. Their physical activity was unrestricted in a ward environment. Blood cimetidine and plasma gastrin were measured in serial blood samples. The nine subjects were treated in random sequence with cimetidine 0-8-1-0 g on one day and placebo capsules on the other. The drug was given in four divided doses: four subjects received it before, and five after, the three main meals. All took the fourth dose at bedtime. Replicate studies in an additional subject given placebo on both study days showed good reproducibility (r=0-80, P less than 0-01). Cimetidine therapy decreased intragastric acidity in all nine subjects. The decrease was similar in the two groups taking the drug before or after meals, mean 24 h intragastric hydrogen ion activity being lowered by 70 and 72% respectively. Nocturnal anacidity was recorded in only two of 45 samples. Administration of cimetidine before meals produced earlier and higher drug blood levels than post-prandial medication, but when it was taken after food the blood levels were highest at the time when the buffer capacity of the food was waning. Blood concentrations of cimetidine exceeded the secretory IC50 level for most of the time between doses. The results show that cimetidine 0-8-1-0 g/day in four divided doses produces a striking and consistent decrease of intragastric acidity. Although variation in the timing of the dose in relation to meals did not affect the decrease of acidity, the absorption data suggest that patients should take the drug after meals.
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PMID:Effect of cimetidine on 24-hour intragastric acidity in normal subjects. 0 61

Measurement of the postprandial rate of acid delivery into the duodenum directly assessed the efficacy of two radically different acid-reducing therapies for duodenal ulcer disease. Cimetidine, 400 mg, with an ordinary solid meal decreased the 4-hr delivery of titratable acid and hydrogen ion into the duodenum by 63 and 86%, respectively (P less than 0.01 versus control). Liquid Maalox, 30 ml, 1 and 3 hr after an identical meal reduced 4-hr delivery of acid by 47 and 74%, respectively (P less than 0.01 versus control). During the study period, the H2 receptor antagonist effected a continuous reduction in gastric acidity and the delivery of acid into the duodenum. The liquid neutralizing antacid produced a more fluctuating decrease in these parameters. However, given in these dosages, the magnitude and duration of the acid-reducing effect were similar for both treatments.
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PMID:Comparison of an H2 receptor antagonist and a neutralizing antacid on postprandial acid delivery into the duodenum in patients with duodenal ulcer. 1 6

The effects of two dose regimens of cimetidine on 24 h intragastric acidity were investigated in six patients with duodenal ulcer. They received placebo capsules on the first day and cimetidine on the second day. Cimetidine 0-8 g/day decreased 24 h mean H+ activity by 55% but 1-6 g/day decreased it by 67%, the difference being due to a greater nocturnal decrease in the high-dose group. Intragastric pH remained below 2-0 for much of the treatment day but similar values were found in four post-vagotomy patients. Cimetidine 0-8-1-6 g/day results in a decrease of intragastric acidity that is compatible with successful medical treatment of duodenal ulceration.
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PMID:24-hour control of intragastric acidity by cimetidine in duodenal-ulcer patients. 5 54

The effect of the histamine H-2 receptor antagonist cimetidine on gastric potential difference (P.D.) has been studied in five healthy volunteers. P.D. was recorded continuously, and basal P.D. (mean +/- S.E.) was -48+/- 1-0 mV. Cimetidine, 300 mg orally, increased P.D. to -64+/- 2-4 mV. Cimetidine also significantly decreased basal acidity from pH 2 to pH 7 within an hour. The effect on both P.D. and pH persisted throughout each 3h study. P.D. has been shown to correlate with changes in the human gastric mucosal barrier. Cimetidine, therefore, may have a protective effect on the gastric mucosal barrier in addition to its suppression of acid secretion.
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PMID:Effect of cimetidine on gastric potential difference in man. 5 55

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 failure of standard oral pancreatic enzyme replacement therapy to correct malabsorption in patients with advanced pancreatic insufficiency is likely due to acid-peptic inactivation of ingested enzymes. Theoretically, the use of cimetidine, an H2-receptor antagonist, in conjunction with oral enzymes, would permit greater transgastric passage of ingested enzymes with resulting improvement in intraluminal lipolysis. To test this hypothesis, we studied the effects of orally administered cimetidine in two groups of patients by utilizing a previously validated double-marker perfusion technique. Cimetidine, in varying doses, had no effect on postprandial exocrine pancreatic function in 16 duodenal ulcer patients without pancreatic disease. In six patients with pancreatic insufficiency, cimetidine produced a pronounced decrease in the output of gastric acid and secretory volume, resulting in reduction of postprandial acidity and intragastric volume. These actions of cimetidine should retard or prevent inactivation of ingested enzymes and also increase their intragastric concentration, with resulting enhancement of luminal duodenal enzyme activity. Supplemental cimetidine may thus be useful in the medical management of patients who fail to respond to routine pancreatic extract therapy alone.
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PMID:Rationale for the use of cimetidine in pancreatic insufficiency. 34 Aug 5

Numerous factors seem to affect zinc absorption. Gastric acid secretion has been demonstrated to facilitate iron absorption. The zinc tolerance test (ZTT with ZnSO4 220 mg p.o.) was performed in 11 healthy volunteers to study the effects of administering the acid secretion inhibitor cimetidine (1 g/day p.o. for 3 days) and to evaluate the influence of HCl gastric secretion on zinc absorption in physiological conditions. Zinc absorption was reduced after cimetidine administration (p less than 0.005), suggesting that gastric pH influences zinc absorption. To rule out any direct effect of the drug on zinc absorption in five other healthy adults we further evaluated zinc absorption by using a different H2 antagonist (ranitidine 300 mg/day for 3 days and 300 mg before the test). Cimetidine was also tested in these subjects at half the dosage administered to the first group of subjects. Gastric acidity was monitored at 60-min intervals throughout the test via a nasogastric tube. The areas under the plasma concentration curves for zinc were significantly reduced after ranitidine (p less than 0.01), but not after cimetidine administration. Gastric acid was also reduced after ranitidine, but not after cimetidine (500 mg) administration, suggesting that gastric acid secretion plays a role in the regulation of zinc absorption in man.
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PMID:Inhibition of gastric acid secretion reduces zinc absorption in man. 189 92

The Authors compared the effects of two H2-antagonist drugs (Famotidine and Cimetidine) on both volume and acidity of gastric secretions. Patients were assigned to three randomized groups, which received respectively: (1) Famotidine 40 mg P.O. the evening before the surgical act; (2) Cimetidine 300 mg P.O. in the same way and Cimetidine 300 mg I.M. 90 min before the induction of anaesthesia; (3) no drug with H2-antagonist effect. Compared with the control group, the treatment with Famotidine and Cimetidine decreases both volume and acidity of the gastric secretions. In the Famotidine group no patient showed pH less than 2.5 and gastric secretions volume greater than 25 ml.
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PMID:[Comparison of the efficacy of famotidine and cimetidine in in prophylaxis of Mendelson's syndrome in elective surgery]. 192 63

The development of effective antisecretory drugs has risen the question of what is the ideal inhibition of gastric acid secretion in the treatment of peptic ulcer. Cimetidine, unlike the more recent H2-blockers and proton pump inhibitors, exerts antisecretory effects that are correlated to the blood levels of the drug. For this reason, therapeutic posologies were initially based on the pharmacokinetic features of the drug, while, more recently, direct measurement of intragastric acidity have assumed great relevance. Despite extensive research, the ideal level of gastric acid inhibition in the treatment of peptic ulcer has not been established. Greater healing rates are achieved by more potent antisecretory drugs and the duration of treatment appears to be also important, particularly to the healing of gastric ulcers. Whether the course of peptic ulcer disease is affected by the potency of the drug employed in the treatment of acute episodes has not been established.
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PMID:Inhibition of gastric acid secretion and therapeutic results: is there any correlation? 198 21

Children undergoing general anesthesia are at increased risk of severe aspiration pneumonitis. Cimetidine and ranitidine, specific histamine (H2-receptor) antagonists, when given 1-3 h preoperatively markedly reduce the acidity and volume of gastric content. A newer compound, famotidine, is a more specific antagonist with no inhibitory effect on the drug metabolizing microsomal enzyme systems of the liver (cytochrome P-450), in contrast to cimetidine. An additional clinical advantage is a possible longer duration of action. In order to evaluate these potential advantages we studied the effects of preanesthetic oral famotidine on gastric fluid pH and volume in 4 groups in a random manner. METHODS. With parental consent, 107 infants and children (ASA I status, 4 months to 14 years old, NPO for at least 6 h) received either no famotidine (n = 29) or 0.15 mg/kg (n = 27), 0.3 mg/kg (n = 25) or 0.6 mg/kg (n = 26) famotidine at 7.00 a.m. Following induction by mask with nitrous oxide/oxygen (N2O/O2) and enflurane (E) or i.v. thiopental, intubation was performed in all patients. Anesthesia was maintained with N2O/O2 and E. A orogastric double-lumen tube was passed into the stomach, and the gastric content was aspirated in a uniform manner. Gastric volume was recorded and pH values were measured with pH paper. RESULTS. In the control group, 28 of 29 patients (97%) had a pH less than 2.5, 18/29 (62%) had a gastric volume greater than 0.4 ml/kg and 17/29 (59%) had a pH less than 2.5 and gastric volume greater than 0.4 ml/kg, meaning an increased risk of pneumonitis if the child aspirates the gastric content. Famotidine administration was effective between 1.5 and 6 h after oral administration. Preoperative famotidine application produces pH values of gastric contents higher than 2.5 in all dosage groups (84%, 94%, 75%), and these differences were highly significant (P less than 0.001), whereas the gastric volume reduction with these doses was not significant. The incidence of pH less than 2.5 and volume of gastric contents exceeding 0.4 ml/kg did not vary with the different doses of famotidine. As there were no measurable differences in the effect of famotidine, we recommend that children at high risk of pulmonary aspiration receive 0.15 mg/kg famotidine orally at least 1.5 h but not later than 6 h before induction.
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PMID:[Famotidine dosage in children. The effect of different doses on the pH and volume of the gastric juice]. 228 7


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