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)

Continuous 24-hour intragastric pH monitoring allows the evaluation of spontaneous late night gastric alkalinization phenomenon (SNA). This nocturnal increase of intragastric pH is strongly evident in healthy volunteers but is insignificant in patients with active duodenal ulcer. Gastric acidity was monitored by 24-hour continuous pH-metry in nine patients with active duodenal ulcer disease before and after two weeks of therapy with ranitidine. A twice daily dose of the drug (150 mg at 08.00 h and 150 mg at 20.00 h) was orally administered to each subject. Before treatment the ulcer patients did not show the SNA phenomenon, but the therapy led it to reappear. Ranitidine significantly reduced the time during which the gastric acidity was lower than 4 pH units; moreover the drug was effective on the ulcer healing during a period as brief as two weeks of therapy. At least a complete healing of the duodenal ulcer could be seen in patients whose overall gastric acidity time was reduced almost to the 40% of the pre-treatment value, meal times excluded from the pH-metric calculation.
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PMID:Twenty-four-hour intragastric pH-metry: H2-receptor antagonist restoration of nightly gastric spontaneous alkalinization in duodenal ulcer healing. 136 62

The effect of gastric acidity on the oral absorption of the quinolone antibiotic enoxacin was evaluated in 12 healthy volunteers. In a randomized, crossover design, single 400 mg oral enoxacin doses were administered on four occasions: alone, after 50 mg intravenous ranitidine, after 2 micrograms/kg subcutaneous pentagastrin, and after combined ranitidine and pentagastrin treatment. Gastric pH was monitored by radiotelemetry capsule for 4 hours after enoxacin administration. Ranitidine pretreatment reduced enoxacin oral bioavailability by an average of 26%. This effect was abolished when pentagastrin was used to maintain low gastric pH. Thus the ranitidine-induced decrease in enoxacin oral bioavailability probably results from a decrease in gastric acidity rather than from an interaction with ranitidine itself.
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PMID:Effect of gastric acidity on enoxacin absorption. 152 81

This controlled study considers the effect of ranitidine, both alone and in association with metoclopramide, on the acidity and volume of the gastric content of 75 patients requiring caesarean section. Ranitidine, when used alone (50 mg intravenously 30-60 minutes before the operation) significantly reduced (p less than 0.01) the acidity (pH greater than 2.5) and the volume (less than 25 ml) of the gastric content of the patient thus treated. Ranitidine in association with metoclopramide may also reduce the pH and the volume, but did not show any significant statistical differences when compared with the use of ranitidine alone.
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PMID:[Pharmacologic prevention of Mendelson syndrome. A controlled clinical trial]. 158 80

This paper reports the use of Ranitidine in preventing upper gastrointestinal tract hemorrhage following thermal injury. In 12 hours after intravenous injection of Ranitidine, gastric pH was elevated from 3.25 +/- 0.26 to 5.16 +/- 0.47 (P less than 0.01) in twenty-one burn patients, with mean TBSA 62.6% +/- 17.2% (31%-87.5%), mean third degree BSA 41.4% +/- 18.3% (0-68%). The volume of gastric secretion was decreased from 15.81 +/- 4.4 ml to 2.85 +/- 0.9 ml. The free acid of gastric secretion was decreased from 25.74 +/- 4.42 mmol/L to 5.98 +/- 3.68 mmol/L (P less than 0.01). The total titratable acidity of gastric secretion was decreased from 44.76 +/- 5.76 mmol/L to 13.85 +/- 0.02 mmol/L (P less than 0.01). Three patients had occult blood in their gastric contents on admission, and it turned negative after Ranitidine therapy. However, during 1987-1988, the incidence of upper gastrointestinal tract hemorrhage of fifty-one patients with similar TBSA and third degree BSA burned was 21.6%. Changes in gastric secretion and lowered incidence of upper gastrointestinal hemorrhage after Ranitidine therapy suggest that Ranitidine may be effective in preventing upper gastrointestinal tract hemorrhage following thermal injury.
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PMID:[Ranitidine in the prevention of upper gastrointestinal tract hemorrhage following thermal injury]. 181 37

Twelve healthy male subjects were dosed with six regimens: ranitidine and De-Noltab (tripotassium dicitrato bismuthate; Gist-Brocades Ltd., Weybridge, England), placebo and De-Noltab, ranitidine and Pepto-Bismol liquid [bismuth salicylate; Procter & Gamble (Health and Beauty Care) Ltd., Egham, England], placebo and Pepto-Bismol, ranitidine and Roter tablets (bismuth subnitrate; Roter Pharma Ltd., Ashford, England), and placebo and Roter. Ranitidine, 300 mg, or placebo was administered at 10 PM (night before) and at 7 AM; at 9 AM, the oral dose of bismuth was either 2 De-Noltabs, 3 30-mL doses of Pepto-Bismol liquid, or 2 Roter tablets. When predosed with placebo, the median integrated 8-hour plasma bismuth concentration was significantly greater after dosing with De-Noltabs than after dosing with either Pepto-Bismol or Roter (61, 8, and 8 ng.h/mL, respectively), with a similar trend for 8-hour median urinary bismuth excretion (213, 40, and 6 micrograms, respectively). When predosed with ranitidine, only after De-Noltab administration were there significant increases in the 8-hour plasma bismuth concentration (147 ng.h/mL), and 8-hour urinary bismuth excretion (686 micrograms). Eliminating intragastric acidity may enhance bismuth absorption after oral dosing with De-Noltabs by maintaining intragastric tripotassium dicitrato bismuthate as a colloidal suspension.
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PMID:The effect of histamine H2-receptor blockade on bismuth absorption from three ulcer-healing compounds. 188 12

Histamine H2-receptor antagonists (H2RAs) often are administered to intensive care unit patients in an attempt to reduce gastric acidity and to prevent stress-related mucosal damage. These agents have an extremely low overall incidence and severity of adverse reactions; however, hemodynamically significant hypotension has been noted. Clinical studies with rapidly administered intravenous cimetidine in critically ill patients have demonstrated a depression in blood pressure in up to 75 percent of patients. Ranitidine, also studied in this setting, does not appear to induce similar hemodynamic changes. The newer H2RAs, famotidine and nizatidine, have not been evaluated in critically ill patients.
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PMID:Hemodynamic effects of H2-receptor antagonists. 198 Jan 82

1. In the isolated vascularly-perfused stomach of the rat, gastrin 1-17 (520 pmol 1(-1)) increased acid output from basal values of 13.7 +/- 2.7 to 92.5 +/- 11.4 mumol h-1 and venous histamine output from 10.1 +/- 2.3 to 54.7 +/- 7.9 nmol h-1 (mean +/- s.e.mean). 2. The H1 receptor agonist 2-methylhistamine (10 mumol 1(-1)) increased acid output to 21.6 +/- 2.9 mumol h-1 (P less than 0.05) and reduced basal histamine output to 4.0 +/- 0.8 nmol h-1 (P less than 0.05). Gastrin-stimulated acid secretion and vascular histamine output was not significantly affected by 2-methylhistamine (10 mumol 1(-1)). 3. The H2 receptor agonist, impromidine, dose-dependently increased basal acid secretion, reaching a maximal value of 145.5 +/- 11.7 mumol h-1 with impromidine (10 mumol 1(-1)), and maximal gastrin-stimulated acid secretion to 167.4 +/- 15.1 mumol h-1 with impromidine (10 mumol 1(-1)). Impromidine dose-dependently inhibited basal and gastrin-stimulated vascular histamine output. 4. The H3 receptor agonist R-a-methylhistamine, (1 and 10 mumol 1(-1)) minimally increased basal acid secretion. R-a-methylhistamine (10 mumol 1(-1)) did not significantly affect maximal gastrin-stimulated acid secretion. Basal and gastrin-stimulated vascular histamine outputs decreased to 4.0 +/- 0.8 (P less than 0.05) and 24.7 +/- 4.7 nmol h-1 (P = 0.05) with R-a-methylhistamine (10 mumol 1(-1)). 5. The H2 receptor antagonist ranitidine (2 mumol 1(-1)) did not inhibit basal acid secretion, but acid outputs with gastrin and all histamine agonists were reduced. Ranitidine did not affect histamine release in the basal state, with gastrin or with any histamine agonist tested. 6 We conclude that gastric histamine release in the rat is regulated via a histamine H2 receptor sensitive to the histamine agonists tested, but not to ranitidine. It is unlikely that the inhibition of histamine release is secondary to increased gastric acidity.
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PMID:Histamine release in the isolated vascularly perfused stomach of the rat: regulation by autoreceptors. 247 Apr 53

Twenty-four-hour intragastric acidity was measured in 10 patients with a past history of duodenal ulcer on the fourth day of dosing with placebo, and either 150 mg ranitidine given twice or four times daily. The order of the treatments was randomized and a double-blind design was employed. Ranitidine (150 mg) b.d. decreased median integrated 24-h intragastric acidity by 65.1%, nocturnal acidity by 89.1%, and daytime acidity by 54.6% (all P less than 0.01 compared to placebo). The corresponding decreases with 150 mg ranitidine q.d.s. were 62.3, 89.9 and 48.8%, respectively (all P less than 0.01) compared to placebo). There were no significant differences between the two dosage regimens of ranitidine (P greater than 0.05). This study shows that giving extra doses of 150 mg ranitidine during the day does not increase the degree of suppression of intragastric acidity.
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PMID:Twenty-four-hour intragastric acidity in duodenal ulcer patients during dosing with placebo, and 150 mg ranitidine twice or four times daily. 252 Jun 20

This study was undertaken to evaluate the effect of various cimetidine and ranitidine administration schedules on intragastric pH in patients with recent episodes of hematemesis. The investigation was performed on 10 subjects whose hemorrhage had ceased either spontaneously or after pharmacological treatment for at least 24-36 h. The following therapeutic regimens were randomly evaluated: bolus infusions of ranitidine (100 mg/6 h and 50 mg/4 h) and cimetidine (400 mg/6 h and 200 mg/4 h) and continuous infusions of ranitidine (0.2 and 0.4 mg/kg/h) and cimetidine (100 mg/h). Each study evaluated at least two consecutive boli or an 8-h continuous infusion. All treatments produced significant elevations in the basal intragastric pH (p less than 0.001). With bolus administrations, however, the pH displayed consistent oscillations. The pH fell below 4 approximately 6 h after the administration in all the patients treated with 400 mg of cimetidine and in three treated with 50 mg of ranitidine. The administration of histamine H2-receptor antagonists every 4 h allowed better control of intragastric acidity. The pH dropped below 4 in seven of the 10 patients in the 4-h period after the administration of 200 mg cimetidine, and in one of the 10 patients treated with 50 mg of ranitidine/4 h. Increasing bolus dose did not reduce the time lapse or increase the inhibition of intragastric acidity. Continuous infusions were efficacious in maintaining pH values constantly above 6. Ranitidine (0.2 mg/kg/h) achieved the same inhibitory efficiency as cimetidine (100 mg/h). These data indicate that continuous venous infusion of both ranitidine and cimetidine is significantly more efficacious than repeated single bolus administrations.
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PMID:Intragastric pH monitoring during antisecretory therapy in patient with gastrointestinal bleeding. 167 Sep 4

The aim of this work is to establish the best treatment for patients with gastric and duodenal ulcer, by measuring the effects of antiacids and H2-receptor antagonists on gastric pH. 16 patients were studied: 9 of them had a duodenal ulcer, 2 a gastric ulcer and 5 had both. All the patients remained fasting and receiving no drug for 24 hrs. During this 24 hrs., a nasogastric tube was inserted into the stomach and the gastric content was obtained by aspiration each hour from 8 A.M. to 8 P.M. Three days after, each patient received a daily dose of 1 g of Cimetidine, and the whole procedure was repeated. The same was done with 300 mg of Ranitidine daily, 150 ml of Al-Mg antiacids daily, and at last, the same procedure was performed with the association of Ranitidine and Al-Mg antiacids at the mentioned dosage. For the statistical analysis of the data, the mean ordinate of the pH was used as a representative value of each individual's pH. Individual differences (pH with treatment minus pH without treatment) were obtained. The mean effect of each treatment was obtained averaging that differences. For comparison among different drugs, the same procedure was used. Student's paired t tests were performed in a signification level. The buffering capacity was measured in the following way: The percentage of the gastric secretion samples with pH equal or higher than 4 in each treatment and in the total number of patients was confronted with the results obtained in the same patients with no treatment. All the drugs were useful for buffering the gastric acidity, but in different intensity. The association of Ranitidine and Al-Mg antiacids showed to be the most efficient statistically when compared with Cimetidine and Al-Mg antiacids; no statistical difference appeared in the comparison with Ranitidine.
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PMID:[In vivo evaluation of the effect of antacids and H2 receptor blockaders on the intragastric pH in gastric and duodenal ulcer]. 287 55


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