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Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Various antacid or antisecretory agents are used to reduce the risk to patients of aspiration of gastric contents during general anaesthesia and a trial of the gastric proton pump inhibitor, omeprazole, is reported here. Twenty women admitted for elective Caesarean section under general anaesthesia received a single 80-mg oral omeprazole dose at 2000 hours on the evening before surgery. Intragastric pH and volume were measured immediately after induction of anaesthesia and on completion of surgery. Eighty-five percent of pH measurements at induction and extubation and 80% and 95% of volume measurements at induction and extubation respectively met the defined success criteria (pH greater than or equal to 2.5, volume less than 25 ml). Omeprazole treatment was well tolerated by the women and Apgar scores and subsequent progress of the babies were acceptable. These results indicate that gastric acidity and volume were acceptable in the majority of women after omeprazole treatment, but the interval from drug administration to induction of anaesthesia may have been too long in some cases and resulted in unacceptably low pHs.
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PMID:Effect of single-dose omeprazole on intragastric acidity and volume during obstetric anaesthesia. 232 24

The pharmacology, pharmacokinetics, clinical efficacy, adverse effects, and dosage and administration of omeprazole are reviewed. Omeprazole, a substituted benzimidazole, has a unique site and mechanism of action because it inhibits the proton pump--i.e., hydrogen, potassium adenosine triphosphatase (H+,K+-ATPase)--and consequently blocks the final common step in the gastric acid secretory pathway. Omeprazole inhibits basal and histamine-, gastrin- and pentagastrin-stimulated gastric hydrochloric acid secretion. It produces a dose-dependent reduction in gastric acidity, gastric acid output, and gastric juice volume and has variable effects on pepsin secretion. Omeprazole has no documented effect on esophageal motility or lower esophageal sphincter pressure. Omeprazole is variably absorbed from the gastrointestinal tract, and food appears to decrease the rate, but not the extent, of drug absorption. The drug is approximately 95% bound to plasma proteins and is metabolized to inactive components that are enterohepatically or renally eliminated. Omeprazole is more effective (in most studies) than H2-receptor antagonists in treating duodenal ulcer, at least as effective in treating benign gastric ulcer, and more effective in treating reflux esophagitis. Omeprazole has been used successfully in patients with Zollinger-Ellison syndrome refractory to treatment with H2-receptor antagonists. Gastrointestinal complaints (nausea and diarrhea) are the most commonly reported adverse effects associated with omeprazole therapy. The most frequently reported laboratory abnormality occurring with omeprazole use is elevation of serum aspartate aminotransferase and alanine aminotransferase concentrations. Omeprazole will serve a valuable role in the management of gastrointestinal tract ulcers and hypersecretory conditions.
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PMID:Therapeutic evaluation of omeprazole. 306 85

The increase in gastrin caused by the gastric proton pump inhibitor, omeprazole, is presumably related to inhibition of gastric acid secretion (GAS). We investigated omeprazole's effect on gastrin release by studying two doses of omeprazole which produced marked acid suppression. Six gastric fistula dogs received omeprazole, 3 mumole/kg, daily for 20 days and, after a rest interval of 2 months, omeprazole, 10 mumole/kg again for 20 days. Both doses of omeprazole increased gastrin levels and produced a decrease in GAS which was still significant (P less than 0.05) 3 days postfinal dose. The increase in the integrated gastrin response by omeprazole, 10 mumole, was greater than by omeprazole, 3 mumole. Omeprazole, 10 mumole, also reduced GAS and gastric acidity, and increased gastric pH more consistently than omeprazole, 3 mumole. The magnitude of the gastrin response corresponded with the degree of acid inhibition and pH increase. Therefore, the data support the hypothesis that the hypergastrinemia caused by omeprazole is dependent on gastric pH and GAS suppression.
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PMID:Omeprazole-induced hypergastrinemia: role of gastric acidity. 373 35

Patients with acute paraplegia from trauma have an increased frequency of developing gastric stress ulceration and subsequent hemorrhage. Current treatment of gastric stress ulcer is by antacids or H2 antagonists, but despite such therapy stress ulceration still occurs, probably because these agents are unable to maintain gastric pH above 4. Omeprazole, which blocks the terminal step of acid secretion--the proton pump, can produce long-lasting achlorhydria. This study examined the efficacy of omeprazole in preventing stress ulcer in rats with acute cervical cord transection. Omeprazole was administered intraduodenally at 1.725, 2.625, 3.5, and 17.5 mg/kg, and the ulcer incidence and gastric acid output were measured. Omeprazole produced a dose-dependent inhibition of gastric acid output in the cervical cord transected rat. At the highest dose, complete achlorhydria was achieved. The quantity of gastric ulceration was inversely proportional to the omeprazole dosage with nearly complete prevention of ulceration at the highest dose. In conclusion, omeprazole is very effective in preventing gastric stress ulcers in the spinal cord transected rat. This appears to be related to its potent long-lasting inhibitory effect on gastric acidity.
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PMID:Effect of omeprazole on acute gastric stress ulceration in cervical cord transected rats. 382 82

Gastric secretion was measured in nine patients with duodenal ulcer before, and after treatment for four weeks with omeprazole 20 mg or 40 mg daily. Basal acidity and acid output were affected variably by 20 mg, but inhibited totally by 40 mg daily. Sham feed stimulated acid output was reduced by 20 mg daily and completely inhibited by 40 mg daily. Maximal pentagastrin stimulated acid output was halved by 20 mg omeprazole daily and 84% inhibited by 40 mg daily. The reduction in acidity was always greater than the reduction of volume. Pepsin output after pentagastrin was little altered but with the reduced secretory volume pepsin concentrations were increased by both doses. The major cause of reduced aspirate acid output after omeprazole is decreased secretion of the primary acid component of the parietal cell by the proton pump H+K+ ATPase. Duodenogastric alkaline reflux is, however, markedly increased after omeprazole and is an additional factor in the resultant hypoacidity or even anacidity after this drug.
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PMID:Basal, sham feed and pentagastrin stimulated gastric acid, pepsin and electrolytes after omeprazole 20 mg and 40 mg daily. 393 37

The chloroplast thylakoid ATPase proton pump-driven H+ accumulation in the dark was compared to the light-dependent proton pump driven by either photosystem II or I, in regard to the effects of the resultant acidity on chemical modification reactions. The assays used to detect the acidity effects were: (a)the incorporation of [3H]-acetic anhydride into membrane protein -NH2 groups, and (b) the effect of a certain level of that chemical modification on inhibition of photosystem II water oxidation activity. Based on labeling data with [3H]-acetic anhydride, 20-30 nmol.(mg chl)-1 of -NH3+ groups appear to be metastable in the dark in untreated membranes. The term metastable is used because proton leak-inducing treatments in the dark lead to about 20-30 nmol . (mg chl)-1 increase in acetic anhydride labeling probably due to reaction with the -NH2 form of amine groups. Addition of low levels of uncoupler or a brief thermal treatment caused a loss of protons from the membrane equivalent to the increase in acetic anhydride derivatization. The increase in acetic anhydride derivatization caused inhibition of water oxidation activity. Using thermally sensitized membranes, photosystem II but not photosystem I electron transport (each giving a steady-state proton accumulation of about 50 nmol H+ . (mg chl)-1 restored the lower level of acetic anhydride reactivity as in previous results (Baker et al., 1981). In dark-maintained, thermally treated membranes, ATPase activity, i.e., the proton pump associated with it, also restored the lower level of acetic anhydride labeling, and again acetic anhydride no longer inhibited water oxidation. Because photosystem I activity did not elicit this type of response to acetic anhydride, there appears to be a pathway for ATPase pumped protons which allows them to reach a restricted domain, perhaps intramembrane, common with the photosystem II water oxidation mechanism and unavailable to protons pumped by photosystem I. The membrane structure(s) which determines this site specificity is not yet understood.
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PMID:Site-specific interaction of ATPase-pumped protons with photosystem II in chloroplast thylakoid membranes. 612 37

A peptic ulcer is a lesion in which acid and pepsin are essential components of pathogenesis. Regardless of the type of patient or the setting in which the ulcer presents, the basic pathogenetic scheme is the same. The primary event is disruption of mucosal integrity. In the presence of acid and pepsin, such disruption of integrity leads to an ulcer. While rarely sufficient by itself to cause ulceration, the presence of acid is a necessary cofactor. The causes of disruption of mucosal integrity include nonsteroidal anti-inflammatory drugs (NSAIDs), Helicobacter pylori and critical illness. With the latter, tissue ischaemia may be the primary event, leading to back-diffusion of H+ ions through increased membrane permeability. Impaired mucosal buffering then leads to intramural acidosis and cell death. Risk factors for bleeding peptic ulcer in the intensive care unit (ICU) include severe trauma, sepsis, respiratory failure, and coagulopathy. Potential roles for decreasing gastric acidity in the treatment of bleeding peptic ulcer include cessation of active bleeding, prevention of rebleeding in hospital and primary prevention of bleeding. Most published studies dealing with the first two situations suggest no benefit with antisecretory therapy. However, the optimal pH for clot and platelet function may be > or = 7.0. Can such pH levels be maintained with antisecretory agents such as the proton pump inhibitors? Are the published trials adequate to demonstrate any benefit from antisecretory agents? Primary prevention of bleeding ulcer in the outpatient setting includes avoidance of NSAIDs, use of antisecretory agents and eradication of H. pylori.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The role of acid in upper gastrointestinal haemorrhage due to ulcer and stress-related mucosal damage. 749 42

Antacids have served us well for over a century. In terms of peptic ulcer disease, the attitude in the late 1950s to 1970s that antacids should be taken only on demand was unjustified and erroneous. 13 recent endoscopic controlled studies have confirmed the efficacy of antacids in the healing of duodenal ulcer, achieving about 75% healing in 4 weeks. The efficacy of antacids in promoting gastric ulcer healing has been less well studied and the results are controversial. The most appropriate and economical antacid regimens for the treatment of duodenal ulcer disease should include tablets or liquid that have acid neutralising capacity of 400 mmol/day given at least an hour after meals. As a long term therapy, antacids appear to work, but need be taken in multiple daily doses, a regimen which is unlikely to meet with long term patient compliance. Patients with gastro-oesophageal reflux disorders or pregnancy-related reflux have also benefited from the usage of antacids ad libitum. Early previous studies have clearly demonstrated the efficacy of antacids in reducing gastro-oesophageal reflux and healing of reflux oesophagitis. The acidity of the gastric contents is the major determining factor in the outcome of the aspiration pneumonitis occurring during delivery. The prophylactic use of antacids during delivery has helped to reduce the severity of this complication. Similarly, the prophylactic administration of antacid aiming to maintain gastric pH between 3.5 to 7.0 has resulted in significant reduction of bleeding due to stress associated ulcers and/or erosive haemorrhagic gastritis in critically ill patients. Antacid therapy, however, is controversial in the management of nonulcer dyspepsia or nonsteroidal anti-inflammatory drug related upper gastrointestinal mucosal damage. Undoubtedly, antacids have major roles to play in the treatment of gastric acid related disorders. They have clear advantages and disadvantages when compared with the antisecretory agents. New proton pump inhibitors in particular have certainly superseded antacids and even the H2-receptor antagonists in many respects. However, the long term safety record of antacids remains unsurpassed by any of the new antisecretory agents.
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PMID:Antacids. Indications and limitations. 751 3

To evaluate endogenous and exogenous factors affecting the quality of ulcer healing produced by proton pump inhibitors, gastric acid pH, serum gastrin, and serum pepsinogen (PG) I and II were measured in peptic ulcer patients before and after treatment with lansoprazole 30 mg once daily. Lansoprazole achieved more rapid scarring in duodenal ulcer (n = 34), with a healing rate of 97.1% after 6 weeks, than in gastric ulcer (n = 56), with a healing rate of 92.8% after 8 weeks. Scarring was the most rapid in gastroduodenal ulcer (n = 8), with a healing rate of 100% after 8 weeks, but the rate of complete scarring was the lowest (37.5%). Lower gastric acidity and lower PG I:II ratio were associated with poor quality ulcer scarring in patients with gastric ulcers, but the opposite was true for those with duodenal and gastroduodenal ulcers. For gastric ulcers, not only ulcer size but also mucosal atrophy was an important factor in ulcer healing. Smoking and alcohol consumption had little effect on the quality of ulcer healing during treatment. These results suggest that there are a number of differences between gastric ulcers and duodenal ulcers in terms of the quality of ulcer healing after lansoprazole treatment.
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PMID:Factors affecting quality of ulcer healing after lansoprazole treatment. 759 44

We studied the gastric acidity, gastric emptying, and proton pump inhibitor (PPI) plasma levels in 10 patients with PPI-resistant ulcers. The pH3 holding-time ratio was low in nine of these patients, with an average ratio of only 39%. PPI plasma levels in those patients were also much lower than in those with nonresistant ulcers. Gastric emptying, determined by the acetaminophen method, was reduced in all 10 patients. Therefore, PPI-resistant ulcers appear to result from insufficient inhibition of gastric acidity, with reduced gastric emptying interfering with the absorption of PPIs. In patients with mild reductions in gastric emptying, PPI plasma levels increased after a change from single-unit enteric-coated tablets (omeprazole) to multiunit enteric-coated granules in capsules (lansoprazole). This change in formulation markedly inhibited gastric acidity and led to rapid healing. In patients with moderate reductions in gastric emptying, doubling the dose of lansoprazole was effective. In patients with severely reduced gastric emptying, there appeared to be a limit to the effectiveness of oral administration of PPIs. Changing the formulation and doubling the dose to compensate for reduced gastric emptying are effective approaches in the treatment of patients with PPI-resistant ulcers.
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PMID:Clinical study on the pathophysiology and treatment of PPI-resistant ulcers. 759 45


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