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

Basal and pentagastrin- or insulin- stimulated secretion was studied in 72 non ulcer dyspectic patients (NUD), in 289 non operated duodenal ulcer patients (DU), and in 30 DU, before and after highly selective vagotomy (HSV). Acidity, proteolytic activity, choline indicating the presence of duodenogastric refluxed material and sialic acid bound to mucus glycoprotein, marker of mucus erosion, were measured. Basal and pentagastrin-stimulated acid and pepsin secretions in NUD were significantly reduced with regard to those in DU. Sialic acid content was weak in basal secretion and markedly increased in response to pentagastrin reaching the values observed in DU. DU basal secretions of acid and of pepsin were modulated according to the stimulating secretory mechanism. Mucus glycoprotein erosion was related to pepsin mucolytic activity and/or to the presence in gastric juice of refluxed material. In DU the increase of peptic mucolysis corresponded to a biological signal of the ulcer attack when no duodenogastric reflux was identified. High values pepsin output in basal secretion and in response to insulin and of basal sialic acid content combined with a pepsin/acid basal output ratio higher than 80 were biological arguments anticipating the efficacy of HSV in DU. Multiparametric analysis of gastric secretion allows to evaluate the ratio between aggressive factors and mucosal defense corresponding to an equilibrium in NUD and to greater aggressivity in DU whose intensity is related to the course of disease.
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PMID:[Gastric functional exploration. Comparison between secretory results in 72 non-ulcer dyspeptic patients and 289 non-operated duodenal ulcer patients. Predictive criteria for the efficacy of fundus vagotomy in duodenal ulcer]. 181 13

Measurement of pH in tissue has shown that the microenvironment in tumors is generally more acidic than in normal tissues. Major mechanisms which lead to tumor acidity probably include the production of lactic acid and hydrolysis of ATP in hypoxic regions of tumors. Further reduction in pH may be achieved in some tumors by administration of glucose (+/- insulin) and by drugs such as hydralazine which modify the relative blood flow to tumors and normal tissues. Cells have evolved mechanisms for regulating their intracellular pH. The amiloride-sensitive Na+/H+ antiport and the DIDS-sensitive Na+-dependent HCO3-/Cl- exchanger appear to be the major mechanisms for regulating pHi under conditions of acid loading, although additional mechanisms may contribute to acid extrusion. Mitogen-induced initiation of proliferation in some cells is preceded by cytoplasmic alkalinization, usually triggered by stimulation of Na+/H+ exchange; proliferation of other cells can be induced without prior alkalinization. Mutant cells which lack Na+/H+ exchange activity have reduced or absent ability to generate solid tumors; a plausible explanation is the failure of such mutant cells to withstand acidic conditions that are generated during tumor growth. Studies in tissue culture have demonstrated that the combination of hypoxia and acid pHe is toxic to mammalian cells, whereas short exposures to either factor alone are not very toxic. This interaction may contribute to cell death and necrosis in solid tumors. Acidic pH may influence the outcome of tumor therapy. There are rather small effects of pHe on the response of cells to ionizing radiation but acute exposure to acid pHe causes a marked increase in response to hyperthermia; this effect is decreased in cells that are adapted to low pHe. Acidity may have varying effects on the response of cells to conventional anticancer drugs. Ionophores such as nigericin or CCCP cause acid loading of cells in culture and are toxic only at low pHc; this toxicity is enhanced by agents such as amiloride or DIDS which impair mechanisms involved in regulation of pHi. It is suggested that acid conditions in tumors might allow the development of new and relatively specific types of therapy which are directed against mechanisms which regulate pHi under acid conditions.
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PMID:Acid pH in tumors and its potential for therapeutic exploitation. 254 40

Indirect pieces of evidences indicate the correlation between insulin level and pathogenesis of peptic ulcer. In the present study, serum insulin releasing level after glucose loading was determined in 16 patients with duodenal ulcer (DU) using radioimmunoassay, and was compared with that of normal controls. The peak insulin level (PIL) in DU patients was significantly higher than that of normal individuals (P less than 0.05), the measurements of gastric acidity, insulin level and the gastroscopic examination were carried out both before and after the treatment. The rebound phenomenon of gastric acidity (BAO) was correlated to that of PIL (r = 0.85). The possible relationship between insulin level and DU was discussed.
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PMID:[Duodenal ulcer and the insulin releasing level]. 269 26

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

Changes on levels gastric acidity, on serum gastrin, cAMP and cGMP levels were studied in 18 healthy volunteers after either stimulation (injection of 0.2 IU of soluble insulin/kg body weight to a group of 9 subjects) or stimulation and inhibition (injection of insulin plus atropine per os to the other group of 9 subjects) of the vagus nerve. After vagus nerve stimulation, gastric acid levels, serum gastrin and cGMP were raised and cAMP reduced. After stimulation and inhibition of vagus nerve, gastrin and cAMP were increased, cGMP reduced and gastric acid levels remained unchanged. These findings suggest that the vagus nerve, and more particularly the acetylcholine released from its metaganglionic fibers, stimulate parietal cells provoking acid secretion, and also stimulate G cells with subsequent gastrin secretion through cGMP.
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PMID:[Secretion of gastric acid, gastrin and cyclic nucleotides in relation to the action of the vagus nerve]. 298 23

Changes of urinary pH, titratable acidity, ammonium, bicarbonate and PCO2, as well as plasma insulin and various plasma and urine electrolytes were studied in 15 normal individuals during a 5-hr glucose tolerance test. After glucose ingestion, urine pH and bicarbonate excretion rose while urine titratable and total acidity, ammonium, Na, K, Cl, phosphorus and PCO2 fell significantly. Serum bicarbonate rose while serum potassium, phosphorus, and anion gap decreased following oral glucose administration. Glucose feeding and the resultant rise in insulin are, therefore, associated with a considerable reduction in urine acidity and Na, K, Cl, and phosphorus excretion. While a significant fall in urinary Na, K and phosphorus has been shown to occur following glucose and insulin administration, their effect on renal H+ excretion in man has not been investigated previously. The mechanism of the observed fall in urine acidity is not clear and requires further investigation.
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PMID:Effects of glucose feeding on renal electrolyte and H+ transport. 299 96

The relation between the basal and stimulated gastric acid secretion, plasma gastrin, and the gastric microflora was examined in 45 patients with rheumatoid arthritis. Sixteen patients (36%) had basal achlorhydria, and of these, 10 (22%) had achlorhydria or hypochlorhydria after stimulation with pentagastrin. The peak acid output and acidity showed inverse correlation with the disease duration but were not associated with age or with the degree of physical disability. Hypergastrinaemia was found in nine patients (20%), of whom 6 (13%) had significant titres of parietal cell antibody. The acidity of the peak acid output showed negative correlation with plasma gastrin. It was confirmed that the gastric secretory state is a determinant of plasma gastrin levels and in addition influences the growth of micro-organisms in the gastric lumen. The type of microflora in the non-acid stomach was similar to that found in the saliva. A subgroup of eight females was identified who showed low gastric acid secretion rates, positive bacterial cultures, and atlantoaxial subluxation. Gastrin- and insulin-like immunoreactivities were found in joint fluid. The concentrations reflected their plasma levels, suggesting that the peptides are not released at the inflammatory site, but rather that they reach synovial fluid from circulating blood.
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PMID:Gastrin, gastric acid secretion, and gastric microflora in patients with rheumatoid arthritis. 352 80

Using model systems, we have studied the properties of a number of zinc-chelating agents which are known to cause diabetes in laboratory animals. The abilities to permeate membranes and to complex zinc inside liposomes with the release of protons are suggested as chemical properties that can enhance diabetogenicity. When such complexing agents are added to lipid vesicles at pH 6 containing entrapped zinc ions, they acidify the contents of these vesicles. We have demonstrated this effect by measuring intravesicular pH both with a fluorine-containing F NMR probe as well as with the fluorescent probe, quinine. For example, using quinine, we observed that 0.1 mM 8-hydroxyquinoline reduced the intravesicular pH of sonicated phospholipid vesicles containing entrapped Zn2+ (as sulfate) from pH 6.0 to 2.8. These diabetogenic chelating agents also solubilized zinc-insulin precipitates from unbuffered suspensions at pH 6.0. The solubilization results from the acidification of these suspensions. Dithizone and 8-hydroxyquinoline at 4 mM solubilized 97 and 42%, respectively, of the suspended insulin. We suggest that if such proton release occurs within the zinc-containing insulin storage granules of pancreatic beta-cells, solubilization of insulin would be induced. Such an event would lead to osmotic stress and eventually to rupture of the granule. The effects of diethyldithiocarbamate (DDC), an agent that has been found to protect rabbits against the induction of diabetes by some other zinc-chelating agents, were also studied. DDC caused a decrease of 3.5 units in the intravesicular pH of zinc-containing vesicles by a mechanism not involving the release of protons upon chelation of zinc. We have demonstrated several properties of DDC which may contribute to its ability to protect against the induction of diabetes. These include its ability to store zinc as a hydrophobic complex in membranes, its consumption of protons upon spontaneous decomposition, and the ability of one of its decomposition products, diethylamine, to accelerate the dissipation of pH gradients across lipid bilayers. Diethylamine is particularly effective in stimulating a rapid dissipation of such pH gradients, even at micromolar concentrations. We have attempted to estimate quantitatively the extent of proton liberation by various zinc-chelating agents. This analysis demonstrated that partitioning of the ligand between organic and aqueous phases, ligand acidity, and zinc complex stability determine the extent of proton release.
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PMID:Mechanism of action of diabetogenic zinc-chelating agents. Model system studies. 388 28

The blood cortisol and gastric acid responses to insulin hypoglycaemia were investigated in 18 healthy control subjects and 14 patients with endoscopically proven duodenal ulceration. In both controls and patients, insulin hypoglycaemia caused blood cortisol and acid output to rise and peak simultaneously, the rises being significantly greater in patients with duodenal ulcer than in control subjects. The peak acid output and the base to peak cortisol increments were also found to be significantly greater in patients with duodenal ulcer than in control subjects (P less than 0.001 and P less than 0.005 respectively). We conclude that insulin hypoglycaemia causes stimulation of the sympathetic and parasympathetic nervous systems and of the hypothalamo-pituitary-adrenal axis, resulting in the simultaneous elevation of gastric juice acidity and blood cortisol levels. We have shown that synchronous rises in gastric acid and blood cortisol occur during insulin hypoglycaemia and that these rises are greater in patients with duodenal ulcer.
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PMID:Measurement of blood cortisol and acid output in patients with duodenal ulceration and normal subjects during insulin hypoglycaemia. 390 8

Hollander's insulin test was evaluated by performing successively partial denervation of the parietal cell area, highly selective, selective, and truncal vagotomy operations on three dogs. The rise in acidity, the timing of the highest rise in acidity, and the rise in acid output were examined. The mean rise in acidity (m-equiv/l) before vagotomy (106 +/- SE11, 120 +/- 23, 60 +/- 16) did not differ significantly from those obtained after partial denervation (67 +/- SE14, 125 +/- 12, 45 +/- 12). After selective vagotomy, a presumed complete denervation, the rises in acidity were significantly lower (0 +/- 0.1, 2.5 +/- 4, 0 +/- 9). The Hollander test, however, was occasionally negative before any nerves had been divided, and was positive in 20% of tests after presumed complete parietal cell denervation. The highest rise in acidity before vagotomy most commonly occurred 30 minutes after insulin, and following partial denervation this rise occurred significantly later, most commonly at 60 minutes. After the other operations there was no consistent timing. The rise in insulin-stimulated acid output after presumed complete denervation provided near complete discrimination between innervated and denervated stomachs, and its repeatability as assessed by the coefficient of variation was significantly better than the repeatability of rise in acidity. These findings provide support for the contention that the results of the insulin test should be expressed quantitatively in terms of the rise in acid output rather than using Hollander-type criteria of changes in acidity.
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PMID:An evaluation of the Hollander test by graded vagotomy in the dog. 474 97


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