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

Intramural pH of the gastric mucosa was measured using a microelectrode technique in rabbit gastric pouches under different secretory conditions and luminal acidity. Exposure of spontaneously secreting or metiamide-treated fundic pouches to a relatively high concentration of luminal acid. HCl 120 mM, for 60 min, led to a marked net loss of luminal H+ which was associated with a significant decrease in the intramural pH (7.28 +/- 0.09 to 6.88 +/- 0.10 and 7.23 +/- 0.07 to 6.99 +/- 0.09, respectively). A linear relationship was observed between the rates of net disappearance of luminal acid and the intramural pH. All 10 spontaneously secreting and five metiamide-treated pouches had superficial mucosal erosions. In contrast, when fundic pouches were exposed to luminal acid in histamine-treated animals, the net loss of luminal H+ was negligible and the intramural pH remained at its base-line level (7.25 +/- 0.07). Histamine stimulation without acid in the lumen caused a small but insignificant increase in the intramural pH (7.27 +/- 0.03 to 7.39 +/- 0.05). Only three of the eight histamine-treated fundic pouches had lesions. In the antral pouches the intramural pH changes in response to exposure to luminal acid were smaller and histamine treatment did not influence the intramural pH. None of the antral pouches had lesions. The results suggest that acidification of the tissue by the diffusion of luminal acid may be an important factor in the pathogenesis of acute gastric ulceration. The acid secretory state of the gastric mucosa can significantly influence the acid-base balance in the mucosa and thus modify its response to acid diffusing from the lumen. Histamine stimulation protected the gastric mucosa by improving its buffering capacity and/or otherwise decreasing the diffusion of H+ from the lumen into the mucosa.
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PMID:Effect of the acid secretory state on intramural pH of rabbit gastric mucosa. 3 Jun 70

Salivary flow rates on mechanical stimulation by forced spitting method and by chemical stimulation with 10% citric acid and gastric acidity using an augmented histamine test were determined in 20 adult patients suffering from duodenal ulcer and in 20 adult control subjects matched with respect to age, sex, and body weight. Salivary flow rates were found to be much higher in response to chemical than to mechanical stimulus in both the groups. Duodenal ulcer patients exhibited an unexplained exaggerated response to chemical stimulation. Salivary pH, amylase, sodium, and potassium levels showed no significant differences between the two groups. The flow rates by either method generally showed a positive correlation with body weight in both the groups. Histamine stimulated gastric acid secretion was higher in duodenal ulcer patients than in controls. Acid secretion did not appear to be related to weight and also showed no consistent correlation with the salivary flow rates. It was concluded that (1) the salivary flow was dependent on body weight in duodenal ulcer patients as well as in controls, and (2) although salivary gland hyperplasia could be postulated in duodenal ulcer patients on the basis of increased salivary flow, the latter was poorly related to maximal acid secretion and therefore, if a combination of parietal cell and salivary gland hyperplasia did exist, it should be considered as incidental.
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PMID:Correlation of salivary and gastric acid secretions in duodenal ulcer patients in tropics. 48 55

Activity of peptic cells is influenced directly by cholinolytic or cholinergic agents. Histamine H2-antagonists influence the activity of the chief cells through changes of acidity of gastric juice.
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PMID:Influence of metiamide and atropine on pepsinogen secretion in the conscious rat. 59 Apr 54

Ketamine exhibited effects on gastric acid secretion total acidity and acid output. Reduction of secretion by ketamine did not appe,r to be significantly different from values obtained with atropine or hexamethonium. In addition to atropine- and hexamethonium-like effects, ketamine also appeared to decrease gastric secretion through a potentiating activity on the sympathetic nervous system. When sympathetic activity was potentiated by cocaine, the antisecretory effect of ketamine appeared to be significantly reduced, compared with that of atropine. Furthermore, after alpha- or alpha- and beta-blockade, ketamine produced similar decreases in secretion, although maximum inhibitory effect was obtained after beta-blockade. Potentiation of adrenergic activity by ketamine seemed to be mediated through alpha-receptors. Histamine H2 receptors did not appear to be involved in the antisecretory action of ketamine.
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PMID:The inhibitory action of ketamine on the rat's gastric secretion. 64 26

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

The effects of 8-week treatment with oral histamine H2-antagonists (ranitidine or cimetidine) or an antacid on plasma levels of histamine and serotonin were studied in duodenal ulcer patients. Histamine H2-antagonists significantly elevated plasma histamine levels, however, they markedly decreased serotonin concentrations by the 4th week of treatment. Antacid treatment similarly increased histamine levels without significantly affecting blood serotonin. It is concluded that changes in intragastric or intraduodenal acidity affect histamine release, as reflected by increased blood levels; serotonin secretion could be influenced by blocking histamine H2-receptors, possibly those located mainly in the gastrointestinal tract.
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PMID:Effects of eight-week treatment with histamine H2-antagonists or an antacid on plasma levels of histamine and serotonin in duodenal ulcer patients. 243 22

Pancreatic enzyme therapy may be beneficial to all patients with chronic pancreatitis, even those in whom the condition is very mild. The goal of enzyme therapy should be to restore normal gastrointestinal physiology as completely as possible. Monitoring of body weight is recommended as the main measure of treatment efficacy. Most pancreatic enzyme preparations presently employed are porcine in origin and must meet certain standards of quality for human consumption. The amount of active lipase in the duodenum determines the quantity of enzymes to be given. An appropriate diet is also important for relieving symptoms of pancreatic insufficiency and improving nutritional status. Although administration of large amounts of proteases has provided pain relief in some patients, the rationale for using enzymes to relieve pain in chronic pancreatitis has not been generally accepted. Gastric acid plays a role in malabsorption, since administered enzymes may be destroyed by gastric acid. Also, acidic conditions in the duodenum decrease the efficacy of pancreatic enzymes administered with meals. Histamine-H2-receptor antagonists may decrease gastric acidity but there are certain drawbacks to long-term use of these agents. The use of enteric-coated microspheres overcomes many of the problems associated with enzyme destruction. Patients with chronic pancreatitis display considerable individual variation in their treatment requirements. Therapy must be tailored to meet the need for adequate disease control as well as for social and emotional acceptability by the patient. The attending physician and the patient share the responsibility for maintaining appropriate therapy.
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PMID:Theory and practice in the individualization of oral pancreatic enzyme administration for chronic pancreatitis. 270 51

The effect of low concentrations of sodium taurocholate on the secretory and electrical activity of isolated rabbit fundic mucosa has been studied. Fundic mucosa maintained a stable potential difference (10.2 +/- 0.6 mV, n = 70) and electrical resistance (85 +/- 6 omega . cm-2, n = 70) and the majority of preparations spontaneously secreted acid (2.85 +/- 0.31 mumol . cm-2 . h-1, n = 70). Histamine (10(-5) and 10(-4) M) and carbachol (10-4 M) increased acid secretion, and these responses were prevented by cimetidine (10(-3) M) and atropine (10(-5) M), respectively. Mucosal application of taurocholate (10(-4) and 10(-3) M) increased net acidity without altering electrical activity. This response exhibited tachyphylaxis, was not altered by pretreating the tissues with cimetidine (10(-3) M), atropine (10(-5) M), or somatostatin (10(-6) M), and occurred in mucosas maximally stimulated by histamine. Sodium thiocyanate (6 x 10(-2) M, serosal side) inhibited spontaneous acid secretion revealing net alkalinization (0.83 +/- 0.05 mumol . cm-2 . h-1, n = 58) that was completely inhibited by anoxia and potassium cyanide (10(-2) M) and markedly reduced by 2,4-dinitrophenol (10(-4) M). Some fundic preparations spontaneously secreted alkali (1.20 +/- 0.20 mumol . cm-2 . h-1, n = 6) after an initial period of acid secretion. Mucosal-side taurocholate (10(-3) M) converted net alkali secretion by both thiocyanate-treated and spontaneously-secreting mucosas to acid secretion without affecting electrical conductance. These secretory responses may be implicated in the pathogenesis of gastric mucosal damage by bile salts.
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PMID:Studies of acid and alkaline secretion by rabbit gastric fundus in vitro: effect of low concentrations of sodium taurocholate. 612 66

Oral FPL-52694 [5-(2-hydroxypropoxy)-8-propyl-4-oxo-4H-1-benzopyran-2-carboxylic acid Na], a new mast cell stabilizer, dose-dependently inhibited gastric acid secretion but increased the volume and pepsin output in pylorus-ligated rats. Intraduodenal FPL-52694 significantly inhibited all of the volume, acidity, acid output and pepsin output. Concerning the acidity, oral administration of the agent showed much more potent inhibition than intraduodenal administration. Oral FPL-52694 markedly inhibited the development of pylorus-ligated ulcers, water-immersion stress- and aspirin-induced gastric erosions and moderately inhibited the formation of reserpine-induced gastric erosions in rats. Intraduodenal FPL-52694 also inhibited pylorus-ligated ulcers whereas it had no effect on aspirin-induced gastric erosions. Histamine-induced gastric erosions were not affected by oral FPL-52694. These effects of FPL-52694 were almost the same as those of cimetidine, except that cimetidine tended to inhibit histamine-induced gastric erosions. Although the precise mechanism of action of FPL-52694 remains unknown, oral FPL-52694 appears to be a promising agent for the treatment of peptic ulcers.
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PMID:Effects of FPL-52694, a new mast cell stabilizer, on gastric secretion and various acute gastric lesions in rats. 654 Sep 73

The present strategies for the management of peptic ulceration are well tolerated and clinically effective. Histamine H2-receptor antagonists can be used for mild to moderate disease, and proton pump inhibitors are of particular benefit for patients with severe peptic ulceration and the Zollinger-Ellison syndrome. However, none of these treatments provides protection against recurrent ulceration, except when taken as long-term continuous treatment. Long-term exposure to pharmacological agents raises problems of safety, particularly relating to a lack of intragastric acidity. In addition, the accelerated development of atrophic gastritis in patients receiving omeprazole requires investigation and assessment. It is unlikely that there will be any major development in the area of control of gastric acid secretion, except perhaps the introduction of specific immunization against gastrin. However, the clinical benefit of this strategy awaits assessment. The main area for development must be the introduction of convenient and effective regimens for the eradication of Helicobacter pylori infection. Existing regimens are either simpler and relatively ineffective, or too complicated for widespread application. Bearing in mind the long gestation period of any new drug, it seems likely that the only innovative drug that will be introduced for the management of peptic ulceration before the millennium will be ranitidine bismuth citrate, an antisecretory anti-H. pylori drug that will usually be used in combination with an antibiotic.
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PMID:Treatment of peptic ulcers from now to the millennium. 794 62


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