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

Pertussis toxin was used to examine the functional linkage between somatostatin and acid secretion and the mode of action of somatostatin at the cellular level in the isolated luminally perfused mouse stomach. Pretreatment of the stomach with pertussis toxin (125-1,250 ng/ml) for 60 min 1) caused a significant twofold increase in histamine-stimulated acid secretion (from 42 +/- 7 to 82 +/- 12 nmol/min; P less than 0.01) but not pentagastrin-stimulated secretion and 2) blocked the inhibitory effect of somatostatin on basal and histamine-stimulated acid secretion but not on pentagastrin-stimulated acid secretion. The ability of pertussis toxin to reverse selectively the inhibitory effect of somatostatin on histamine-stimulated acid secretion is consistent with the ability of pertussis toxin to inactivate a guanine nucleotide binding protein, which couples somatostatin receptors to inhibition of adenylate cyclase; histamine, but not gastrin, stimulates acid secretion via activation of adenylate cyclase. Secretagogue-stimulated acid secretion was accompanied by a parallel increase in somatostatin secretion that is largely determined by luminal acidity. The augmentation of histamine-stimulated acid secretion after treatment with pertussis toxin implied that the concomitant increase in somatostatin secretion is coupled to acid secretion and acts to attenuate it. The results confirm the role of gastric somatostatin as a paracrine regulator of acid secretion.
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PMID:Linkage between somatostatin and acid secretion: evidence from use of pertussis toxin. 256 28

In a double-blind, placebo-controlled study of SK&F 94482 (BMY-25368) (400-mg, post-evening meal, for 7 days in 11 healthy subjects), there was a significant 75% decrease in median integrated 24-h intragastric acidity during dosing with the drug (218 mmol h/L) compared with placebo (883 mmol h/L; P = 0.003). The single daily dose of 400 mg SK&F 94482 decreased median hourly intragastric acidity until the time of the next dose 24 h later. There was also a sustained and significant 80% rise in median 24-h integrated plasma-gastrin concentration during dosing with SK&F 94482 (364 pmol h/L) when compared with placebo (202 pmol h/L; P = 0.003). The study demonstrates a significant inverse correlation between 24-h integrated intragastric acidity and 24-h plasma gastrin concentration (rs = -0.484; P less than 0.001). The study shows that a single oral daily dose of an H2-antagonist can provide control of intragastric acidity throughout the day and night, decreased acidity being associated with statistically significantly, but modestly elevated plasma-gastrin levels.
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PMID:The effect of SK&F 94482 (BMY-25368) on 24-hour intragastric acidity and plasma gastrin concentration in healthy subjects. 257

I.v. administration of neurotensin and its analogue DTch1I--neurotensin considerably decreased stomach secretion induced with pentagastrin but did not suppress stomach secretion induced with histamine, neither a microapplication of 10 micrograms in 3 microliter of neurotensin affected the secretion whereas the dose 50 micrograms in 3 microliter decreased both volume and acidity of the juice. I.v. administration of neurozensin increased the gastrin, neurotensin and the substance P contents in the dog blood. Microapplication of neurotensin to the globus pallidus with simultaneous i.v. administration of histamine increased the level of the serum gastrin.
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PMID:[Effect of natural neurotensin and its analog on gastric secretion and levels of various peptides in dog blood]. 258 Jul 44

The interrelations among fasting serum gastrin, serum creatinine, gastric acid secretion variables, and G-cell densities were analyzed in 47 patients with chronic renal failure (CRF). The patients also underwent gastroscopy and radiologic upper gastrointestinal barium examination. It is suggested that the hypergastrinemia seen in CRF is related to several factors: gastric acidity, grade of renal failure, G-cell density, and basal gastrin secretion rate. With regard to serum gastrin two different populations can be found, the cutting-off point being 300 ng/l. Although the group with high gastrin levels included significantly more patients with gastric body atrophy than the other group (4 of 11 versus of 1 of 36), most of them had no atrophy, which indicates that (an)other mechanism(s) is responsible for the hypergastrinemia. In the relation between serum gastrin and gastric acidity also, two differently behaving subgroups emerged. In the first, strong acidity change corresponded to minor gastrin change, whereas in the other, minor acidity change corresponded to marked gastrin change. The correlation coefficients between gastrin and acidity were high within both subgroups. During regular dialysis patients preserve the characteristics delineated from non-dialyzed values. Patients with signs of duodenal ulcer disease had high maximal acid output and low serum gastrin. Otherwise no associations were found between GI findings and the variables studied.
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PMID:Serum gastrin in chronic renal failure: its relation to acid secretion, G-cell density, and upper gastrointestinal findings. 259 56

Single doses of omeprazole inhibit pentagastrin-stimulated gastric acid secretion and almost complete inhibition can be achieved for 4-6 hours with a single dose of 80 mg. Acid secretion then slowly returns and reaches normal levels after 3-4 days. Omeprazole also dose-dependently inhibits basal acid secretion as well as acid secretion stimulated with histamine, peptone and modified sham feeding, with similar efficiency. During repeated once-daily dosing with an enteric-coated granule capsule formulation, inhibition of acid secretion increased initially, and stabilized within about 4 days. Dose-response studies in patients with duodenal ulcers and healthy subjects have shown that 20-40 mg/day results in a peak reduction (80-100%) of pentagastrin-stimulated acid secretion 6 hours after dose. Studies of 24-hour intragastric acidity in duodenal ulcer patients have shown that 4 weeks of treatment with omeprazole, 20 mg once daily, resulted in a reduction of median intragastric acidity by 97%, which was superior to the 57% median reduction achieved with ranitidine, 150 mg b.d., for 4 weeks in the same patients. During omeprazole treatment, fasting plasma gastrin increased in relation to the degree of inhibition of acid secretion. After discontinuation of treatment, plasma gastrin normalized. Treatment with omeprazole, 20 mg, increased 24-hour plasma gastrin to the same extent as after highly selective vagotomy. Long-term treatment with omeprazole, 20-40 mg, for up to 2 years has not been associated with any progressive rise in fasting plasma gastrin.
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PMID:Effect of omeprazole on gastric acid secretion and plasma gastrin in man. 269 Mar 29

Omeprazole is the first H+-K+-adenosine triphosphatase antagonist available for clinical use. It has a very strong, long-lasting inhibitory effect on gastric acid secretion. The effect is very selective: pepsin and intrinsic factor secretion are unaffected. Once-daily doses of 30-40 mg cause a more than 95% reduction of intragastric acidity. Lower doses have less predictable results. During treatment with omeprazole serum gastrin levels increase. After cessation of treatment gastric acid secretion and serum gastrin levels rapidly return to pretreatment levels. No rebound phenomena are observed after treatment.
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PMID:Effects of omeprazole on gastric secretory functions. 269 7

Thirty patients with bile reflux gastritis, proven by gastroscopy and Milk 99mTc-EHIDA Test, were studied and their clinical features were compared with those of patients with non-bile reflux gastritis. The symptoms were similar in both groups of patients, whereas histologically in bile reflux gastritis there were more hyperemia of mucosa, more obvious edema in lamina propria and more polymorphonuclear infiltration. Furthermore, in bile reflux gastritis the histological changes were more severe in the antrum and decreased in severity toward the cardia. Acid secretion was significantly lower in patients with bile reflux gastritis than in patients with non-bile reflux gastritis while the serum gastrin level was significantly higher in the former than in the latter group. The authors suggest that there may be a vicious cycle among duodenogastric reflux, low level of gastric acidity and high level of serum gastrin. When duodenogastric reflux occurs, not only the bile salts damage the gastric mucosa and subsequently cause the back diffusion of hydrogen ion but also the alkaline duodenal juice neutralizes the gastric acid, resulting in decrease of gastric acidity. The bile salts and low acidity can stimulate the release of serum gastrin which antagonizes the effects of cholecystokinin and secretin on pyloric tone and aggravates the duodenogastric reflux.
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PMID:[Clinical characteristics of bile reflux gastritis]. 273 41

To evaluate the neural regulation of postprandial somatostatin release we studied the effect of blockade of (a) alpha-adrenergic and beta-adrenergic and (b) cholinergic receptors on the plasma somatostatin, gastrin and insulin responses to a standard meal in two groups of five fasting healthy male volunteers. Thymoxamine (0.1 mg/kg iv over two minutes then 10 mg/hour for two hours) and propranolol (0.15 mg/kg iv over two minutes, then 0.75 mg/kg/hour for two hours) were started just before eating while atropine (0.04 mg/kg/im) was given at 15 minutes on completion of the meal. There was a prompt and sustained rise in plasma somatostatin after a control meal in all experiments. This rise was arrested by atropine but not altered by either thymoxamine or propranolol. The plasma gastrin response to a meal was moderately enhanced by thymoxamine and markedly enhanced by atropine. Postprandial insulin release was not affected by alpha- or beta-adrenergic blockade but was abolished by atropine. The effect of atropine on the postprandial plasma somatostatin rise might have been mediated through reduction in gastric acidity or delay in gastric emptying. Hence we gave five fasting male volunteers and intraduodenal infusion of fat emulsion (25 calories in 30 minutes) on two occasions both alone and after atropine. Plasma somatostatin rose during the fat infusion alone and this rise was abolished by atropine. These data suggest that (a) cholinergic but not adrenergic mechanisms are important modulators of plasma somatostatin release after orally ingested and intraduodenally infused nutrients (b) atropine abolishes plasma somatostatin release independently of its effects on gastric acidity and motility and (c) are consistent with the hypothesis that atropine potentiates postprandial gastrin release through reduction of somatostatin mediated inhibition.
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PMID:Autonomic regulation of postprandial plasma somatostatin, gastrin, and insulin. 286 95

Renal gastrinoma has not been previously reported. A 12-year-old boy with Zollinger-Ellison syndrome was found to have a renal tumor. No other tumor was detectable by imaging techniques, and selective venous sampling for gastrin showed a significant renal vein to vena cava gradient. Nephrectomy was performed, and examination of the tumor showed typical histologic features of an endocrine tumor. G cells were apparent by electron microscopy, and immunoperoxidase staining for gastrin, neuron-specific enolase, and chromogranin were positive. The gastrin content was unusually low for gastrinomas: 128 pg/g. Following nephrectomy, fasting gastrin and secretin stimulation testing were normal. Basal acidity was reduced by 60% but remained elevated at 39 mmol H +/h (hydrogen ion per hour). We speculate that renal gastrinoma may be characterized by uniquely poor gastrin storage and that curative resection of all gastrinoma tissue may not necessarily be associated with immediate complete suppression of hyperacidity.
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PMID:Zollinger-Ellison syndrome associated with a renal gastrinoma in a child. 287 87

In the present study the effect of indomethacin-induced prostaglandin deficiency was examined on the release of bombesin-like immunoreactivity (BLI), a putative peptidergic neurotransmitter, from the isolated perfused rat stomach. In addition, gastrin and somatostatin (SLI) secretion was determined. Pretreatment of rats with indomethacin (2 mg/kg X h) resulted in a 3-fold increase of basal BLI secretion. In response to acetylcholine (2 X 10(-6) M) BLI rose from 2,000 to 4,000 pg/min, whereas in controls BLI increased from 400 to 1,400 pg/min. While absolute values for BLI secretion were higher in indomethacin-treated stomachs the relative increase above baseline was lower (100 vs. 250%). In control rats the increase in BLI secretion in response to acetylcholine was abolished when the acidity in the gastric lumen was increased from pH 7 to pH 2. After indomethacin, however, the stimulatory effect of acetylcholine during luminal pH 7 and pH 2 was identical. The decrease of SLI by acetylcholine at luminal pH 7 was abolished in indomethacin-treated stomachs in response to 10(-6) M acetylcholine, and 2 X 10(-6) M had even a stimulatory effect on SLI secretion. Indomethacin pretreatment reduced gastrin secretion at luminal pH 7. These data demonstrate that endogenous prostaglandins exert an inhibitory tone on basal and stimulated BLI and stimulated SLI secretion in the rat stomach. It is suggested that endogenous prostaglandins also inhibit the release of a peptidergic neurotransmitter, similar to their effect on the classical neurotransmitters acetylcholine and norepinephrine.
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PMID:Effect of indomethacin on bombesin-like immunoreactivity, somatostatin and gastrin secretion from rat stomach. 288 61


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