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

In studies with piglets of the country race the applicability of variously treated straw materials was tested in comparison with conventional concentrate feeding (I) after an early weaning date (30th-35th day of life) over an 8-week period (1st-8th week of keeping). In the rations containing 10% straw (straw-concentrate mixtures), untreated (II), HCl treated (III: HCl treatment without steaming) and partly hydrolyzed straw meal (IV: HCl treatment with subsequent steaming) were used in the feeding. Samples were taken of 4 killed animals each in the 2nd and 8th weeks of keeping for the qualitative histologic assessment of palatum durum, oesophagus and stomach, duodenum and caecum, colon ascendens, colon descendens and rectum. Although significantly lower pH values in the stomach were registered after the feeding of feed mixtures III and IV due to increased acidity (pH value decrease by 1.3 to 1.5 units) in comparison to the values in I and II, the lamina epithelialis of the palatum durum remained intact in all groups and without any signs of cauterization. Equally, considerable changes in the comparison of the feeding groups could not be detected in the structures of the oesophagus and the stomach walls or in the qualitative histologic assessment of the duodenum and the caecum. However, there were clearly distinguishable group specifics with regard to the formation of lymphoreticular tissue in the stomach and for the colon ascendens.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The applicable merit of untreated, HCl-treated and partly-hydrolysed straw meal in the feeding regimen of piglets after early weaning. 4. Histological findings in the digestive epithelium of the piglet]. 261 51

Cerebral lactic acid, a product of ischemic anaerobic glycolysis, may directly contribute to ischemic brain damage in vivo. In this study we evaluated the effects of extracellular acid exposure on 7-day-old cultures of embryonic rat forebrain. Mixed neuronal and glial cultures were exposed to either lactic or hydrochloric acid to compare the toxicities of relatively permeable and impermeable acids. Neurons were relatively resistant to extra-cellular HCl acidosis, often surviving 10-min exposures to pH 3.8. In the same cultures, immunochemically defined astrocytes survived 10-min HCl exposures to a maximum acidity of pH 4.2. Similarly, axonal bundles defasciculated in HCl-titrated media below pH 4.4, although their constituent fibers often survived pH 3.8. Cell death occurred at higher pH in cultures subjected to lactic acidosis than in those exposed to HCl. Over half of forebrain neurons and glia subjected for 10 min to lactic acidification failed to survive exposure to pH 4.9. Longer 1-h lactic acid incubations resulted in cell death below pH 5.2. The potent cytotoxicity of lactic acid may be a direct result of the relatively rapid transfer of its neutral protonated form across cell membranes. This process would rapidly deplete intracellular buffer stores, resulting in unchecked cytosolic acidification. Neuronal and glial death from extracellular acidosis may therefore be a function of both the degree and the rapidity of intracellular acidification.
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PMID:The effects of extracellular acidosis on neurons and glia in vitro. 273 13

Aspirin induces gastric mucosal damage in animals and humans. The purpose of this study was to examine whether cimetidine protects the human gastric mucosa from acute aspirin-induced damage. Eight healthy subjects were studied on 4 separate days. Cimetidine, 400 mg, or placebo was given orally 1 hour before initial endoscopy. The stomach was isolated and atropine given to suppress basal acid secretion. Each study consisted of four 15 min periods during which an acidic test solution was instilled into the stomach. During the second period only, either aspirin (1300 mg, 36 mmol) or control for aspirin (36 mmol HCl) was added to the test solution. Ion fluxes and gastric mucosal potential difference were measured, and endoscopy performed following each test. After placebo, aspirin significantly altered hydrogen ion flux and potential difference versus basal and control. Cimetidine decreased the damaging effect of aspirin. Endoscopic scores increased after aspirin plus placebo, whereas they remained unchanged after aspirin plus cimetidine. Therefore, cimetidine decreased aspirin-induced gastric mucosal damage in humans. As gastric acidity was identical during all studies, the effect of cimetidine was independent of gastric acid secretion.
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PMID:Cimetidine decreases aspirin-induced gastric mucosal damage in humans. 297 81

Nizatidine is a potent and selective antagonist of histamine. The histamine-induced relaxation of the KCl-treated rat uterus was inhibited dose-dependently by nizatidine. The inhibition was characterized by displacement of the dose-response to histamine to the right, in parallel, without depression of the maximum. The affinity of nizatidine for the histamine H2-receptor of the rat uterus was about 10 times that of cimetidine. The steady-state dose-response acid outputs stimulated by histamine from the Heidenhain pouch and the gastric fistula were also shifted dose-dependently by nizatidine, in parallel, to the right. The inhibition was consistent with a surmountable antagonism of histamine. At high (10(-4) to 10(-3) M) concentrations, nizatidine increased the motility of the guinea pig stomach and duodenum in vitro; this effect was abolished noncompetitively by atropine (10(-8) M) and pyrilamine (10(-4) M). Both nizatidine and cimetidine administered s.c. showed "cytoprotective" action by reducing the gastric lesions induced by 1) aminoguinidine and pylorus ligation and 2) HCl plus aspirin in the rat. On a weight and molar basis, nizatidine was 4 and 5.25 times as effective as cimetidine, respectively. This cytoprotective action of nizatidine was found when acidity and total acid load in the stomach were not affected by the histamine H2-receptor antagonist.
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PMID:Actions of nizatidine on the rat uterus, dog stomach and experimentally induced gastric lesions. 309 39

Evidence has been accumulating that conditions of nonphysiological pH may affect the results of in vitro genetic tests by mechanisms unrelated to the chemical being tested. Medium was pH-adjusted with HCl, NaOH or with organic buffers (Good's zwitterions). In the absence of S9 mix, no changes in mutant frequency were observed over a pH range of 6.4-9.2; a small, 1.9-fold increase was observed for a moderately toxic treatment (24% relative growth) at pH 6.3. However, in the presence of S9 mix, the mutant frequency increased sharply for pH values below 6.8. At pH 6.4, a 4-fold increase was induced, and pH 6.0 resulted in a 10-fold increase in mutant frequency. Basic pH shifts in the presence of S9 mix caused no changes in mutant frequency up to pH 8.0; treatment with pH 8.8 was highly toxic (5.3% relative growth) and caused a 3-fold increase in mutant frequency. Thirteen mutant clones induced at pH 6.0 with S9 mix were challenged with trifluorothymidine after their expansion in nonselective medium and all retained their resistance; another 14 clones were tested for thymidine utilization and all incorporated only 0.1-5.5% of the 14C-labeled thymidine used by the parental line. The induced mutants were primarily of the small-colony phenotype, which indicated clastogenic activity. This was confirmed with chromosome studies which showed a large increase in cells with aberrations consisting of chromatid breaks and complex rearrangements. The results show that the combination of weak acidity (pH 6-6.8) and S9 mix is mutagenic and clastogenic to L5178Y TK+/- cells.
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PMID:Effect of pH shifts on the mutant frequency at the thymidine kinase locus in mouse lymphoma L5178Y TK+/- cells. 311 28

To assess the effect of malnutrition on gastric acidity and gastric bacterial colonization, we studied 35 severely malnourished Bangladeshi children before (0 wk) and after (3 wk) they received nutritional rehabilitation for 3 wk. These results were compared with those obtained from a similarly examined group of 20 better-nourished Bangladeshi children. Gastric acid output, both basal and after betazole stimulation, was significantly lower in the malnourished group at 0 wk compared with the better-nourished children (p less than 0.01): basal 0.22 vs. 0.52 mEq HCl/h and stimulated 0.90 vs. 2.5 mEq HCl/h. Both the concentration of acid and the rate at which gastric juice was secreted were decreased in the malnourished group but serum gastrin levels were not significantly different. After 3 wk, the malnourished children had improved from 61% (+/- 9.0%; SD) to 81% (+/- 8.1%) of expected weight-for-height and were not significantly different than the better-nourished group (86% +/- 11%). Nevertheless, gastric acid concentration remained depressed in the 3-wk group, although the rate of gastric juice secretion equaled levels observed in the better-nourished group. None of the better-nourished children had detectable gram-negative bacterial colonization of their gastric juice. In contrast, 26 of 32 (81%) malnourished children at 0 wk were colonized--even after betazole stimulation, 11 of 33 (33%) gastric juice samples yielded viable organisms--suggesting that the decrease in gastric acid output greatly reduced the gastric acid barrier. Interestingly, only 9 of 20 (45%) better-nourished children had gastric juice with basal pH values below 4.0, suggesting that the gastric acid barrier may be an intermittent defense factor in Bangladeshi children.
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PMID:Decreased gastric acid secretion and bacterial colonization of the stomach in severely malnourished Bangladeshi children. 312 29

We measured gastric mucus pH in vivo in a canine chambered stomach preparation using glass pH microelectrodes. The average maximum mucus pH was 6.52 at a luminal pH of 3.0, declining gradually as luminal pH was lowered; the mucus pH gradient was obliterated completely when luminal pH reached 1.1. At a luminal pH of 1.0, the average maximum mucus pH increased to 6.03, whereas transmural potential dropped from -50.3 to -31.8 mV. Prostaglandin E2 pretreatment (10 micrograms/ml) prevented epithelial injury during exposure to 100 mM HCl, but mucus pH was unchanged as compared with the acid-only group (4.77 vs. 4.72, p = 0.92). Histology on stomachs exposed to a luminal pH of 1.0 revealed characteristic changes of superficial epithelial injury without affecting the deeper gastric glands or disrupting the basal lamina. Prostaglandin E2 pretreatment prevented these histologic changes. These results indicate that although the mucus pH gradient can be overwhelmed by high luminal acidity, a newly formed mucus pH gradient may develop after disruption of epithelial integrity, possibly providing protection for the mucosa during the period of epithelial repair. The high mucus pH (4.77) accompanying normal histology and unchanged potential suggests that prostaglandin E2 may protect the surface epithelium by the stimulation of bicarbonate secretion.
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PMID:In vivo measurement of gastric mucus pH in canines: effect of high luminal acidity and prostaglandin E2. 292 71

The effect of experimental acidification on mercury methylation, demethylation, and volatilization was examined in surficial sediment samples from a weakly buffered northern Wisconsin lake. All mercury transformations were measured with radioisotopic tracers. Acidification of sediment pH with H2SO4, HCl, or HNO3 significantly decreased 203Hg(II) methylation. Acidification of pH 6.1 (ambient) sediments to pH 4.5 with either H2SO4 or HCl inhibited methylation by over 65%. The decreased methylation was due to the increased hydrogen ion concentration because methylation was not affected by concentrations of Na2SO4 or NaCl equimolar to the amount of acid added. Inhibition of methylation was observed even after prolonged acidification of sediments to pH 5.0 for up to 74 days. Acidification of sediments to pH 5.5, 4.5, and 3.5 with HNO3 resulted in a near complete inhibition of methylation at each pH. Similarly, the addition of equimolar amounts of NaNO3 resulted in a near complete inhibition of methylation, indicating that the inhibition was due to the nitrate ion rather than to the acidity. Demethylation of methyl mercury was not affected by pHs between 8.0 and 4.4, but sharply decreased below pH 4.4. Volatilization of 203Hg(II) from surface sediments was less than 2% of methylation activity and was not significantly different from that in killed sediments. This study indicated that acidification of sediments inhibits mercury methylation and that the observed increase in the mercury burdens in fish from low pH lakes is not due to increased production of methylmercury in sediments.
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PMID:Effects of acidification on mercury methylation, demethylation, and volatilization in sediments from an acid-susceptible lake. 317 8

The effects of gastric secretagogues on 0.6N HCl-induced gastric lesions and gastric mucosal prostaglandin E2 (PGE2) contents were investigated in rats. Secretagogues such as histamine (Hist) and amogastrin (Gast) significantly inhibited the formation of gastric lesions induced by 0.6N HCl. The time course of the gastric protective effect of these secretagogues paralleled the increase of gastric acid secretion. This increase was due to the increase in acidity, not to the volume of the gastric juice. The gastric protective effects of Hist and Gast were inhibited by pretreatment with cimetidine, timoprazole and indomethacin. Hist and Gast caused an increase of PGE2 contents in gastric mucosa. These increases were inhibited by the administration of cimetidine and timoprazole. Carbachol (CCh), however, did not have any gastric protective effect; nor did it have any effect on PGE2 contents. CCh caused an increase of acid secretion due to the increase of the volume of gastric juice, but not to an increase in acidity. These results suggest that the gastric protective effect of Hist and Gast, induced by the increase of acidity in gastric juice, is due to the endogenous PGE2 synthesized by the stimulation of acid in the gastric mucosa.
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PMID:Gastric protective effects of gastric secretagogues on 0.6N HCl-induced gastric lesions in rats. 324 41

Cysteamine is widely used in rodents to induce duodenal ulcer. Herein, the pathogenesis of duodenal ulceration in its earliest stages was reviewed using findings from cysteamine- and propionitrile-induced duodenal ulcer in rodent models, especially taking into account changes in the secretion of gastric acid, duodenal and pancreatic bicarbonate as well as gastroduodenal motility. The effect of cysteamine-HCl in inducing ulcers in rats is circadian rhythm-dependent. The effect is greatest from just before the end of diurnal rest to just after the start of nocturnal activity. The chronobiologic effect may be in part due to the circadian rhythm-dependent increased gastric acid production from cysteamine. Titratable acidity was found to be twice as great in the gastric juice of rodents when cysteamine was given by injection at 2000 (just after the start of nocturnal activity) in comparison to when given at 0800 or 1200 (at the beginning or middle span of daily rest). Further studies have shown that adrenalectomy of rats 7 days before cysteamine administration obliterated the observed circadian susceptibility to ulcer formation. Duodenal ulceration, at least in the cysteamine model, appears to be under chronobiologic neuroendocrine control or influence, seemingly mediated by the adrenal glands.
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PMID:Development and significance of cysteamine and propionitrile models of duodenal ulcer. 331 59


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