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Adenosine deaminase activity in the human duodenal mucosa in relation to gastric acid secretion

100%

Namiot Z., Stasiewicz J., Marcinkiewicz M., Gorski J.

Journal of Physiology and Pharmacology

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1992

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tom 43

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nr 2

Adenosine deaminase (ADA) activity was estimated in mucosal specimens obtained endoscopically from the duodenal bulb. Three groups of subjects were studied: 1. 9 patients with achlorhydria, 2. 12 subjects with normal gastric acid secretion, 3. 5 patients with hypersecretion. Enzyme activity was measured by determination of ammonia liberated from the substrate according to the Chaney and Marbach method. In patients with hypersecretion the ADA activity was lower than in those with achlorhydria (p < 0.001) and normal acid secretion (p < 0.02). A significant negative correlation between ADA activity in the duodenal bulb mucosa and basal and maximal gastric acid outputs was found. The present study seems to indicate a possible relationship between gastric acid secretion and duodenal ADA activity.

2

The effect of jejunoectomy on alkaline phosphatase activity in the ileum

86%

Gawlik Z., Nutzenadel W., Krawczyk M., Wiśniewska I. E.

Folia Histochemica et Cytobiologica

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1985

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tom 23

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nr 3

3

Factors influencing the restitution of the duodenal and colonic mucosa after damage

72%

Riegler M., Feil W., Wenzl E., Schiessel R.

Journal of Physiology and Pharmacology

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1991

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tom 42

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nr 1

Rapid epithelial restitution is an important protective mechanism which enables the gastrointestinal mucosa to reestablish epithelial integrity following superficial injury within hours. In this study we examined the influence of an acidic luminal pH, removal of the necrotic layer, nutrient bicarbonate, calcium and sodium desoxycholate (Na-DOC) on restitution in the rabbit duodenum in vitro and the role of Na-DOC and calcium for rapid restitution of the human colon in vitro. Transmucosal potential difference (PD), short-circuit current (lsc) were measured and resistance against passive ion flux (R) was calculated. Electrophysiological changes paralleled morphological injury but did not necessarily reflect restitution in all experiments. The extent of mucosal injury was assessed by computerized real-time morphometry. 5 hrs after luminal exposure to 10 mH HCl for 10 min residual damage (RD) was 14% in the duodenum. Luminal pH of 3.0 (RD of 30%), removal of necrotic layer at acidic luminal pH (RD of 66%), absence of bicarbonate from the serosal solution (RD of 35 % at neutral luminal pH; RD of 96% at acidic luminal pH) and removal of calcium from the serosal solution (RD of 58 %) impaired restitution in the duodenum. Continuous postinjury luminal Na-DOC exposure did not influence restitution in the duodenum (RD of 19%). 5 hrs after luminal exposure to 0.5 mM Na-DOC for 10 min RD was 26% in the human colon. Continuous postinjury luminal Na-DOC exposure (RD of 51 %) and removal of calcium from the nutrient solution (RD of 65 %) impaired restitution in the human colon. Thus we conclude that restitution of the rabbit duodenum in vitro requires a necrotic layer and bicarbonate flux to withstand acidic luminal pH, while restitution is not Effected by Na-DOC. In the human colon Na-DOC inhibits restitution. Both the duodenum and colon require calcium for rapid restitution.

4

Gastric and duodenal mucosa in children with duodenal ulcer before and after eradication of Helicobacter pylori

72%

Bak-Romaniszyn L., Planeta-Malecka I., Kulig A., Czkwianianc E., Suski S.

Journal of Physiology and Pharmacology. Supplement

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1997

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tom 48

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nr 1

5

Acid-sensing protective mechanisms of duodenum

58%

Kaunitz J. D., Akiba Y.

Journal of Physiology and Pharmacology. Supplement

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2003

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tom 54

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nr 4

19-26

The proximal duodenal mucosa, exposed to frequent pulses of gastric acid, is functionally "leaky", increasing the importance of defense mechanisms such as the mucus gel layer, cellular acid/base transporters, bicarbonate secretion, and mucosal blood flow. Our laboratory has used a unique in vitro perfused microscopic system to measure thickness of the adherent mucus gel (MGT), intracellular pH (pHi), bicarbonate secretion, and mucosal blood flow in anesthetized rats. Exposure to pulses of luminal acid, mimicking the rapid physiologic shifts of luminal pH, increases MGT and blood flow, and induces cellular bicarbonate loading, the latter followed by augmented bicarbonate secretion. The mechanism by which the epithelium senses luminal acid includes capsazepine-inhibitable vanilloid receptors, presumably similar to the vanilloid receptor TPVR-1. CFTR, the cAMP-regulated anion channel mutated in the disease cystic fibrosis, plays an essential role in duodenal bicarbonate secretion. Our data are consistent with the hypothesis that cellular bicarbonate loading is an important means of preserving epithelial pHi during luminal acid challenge. Increased MGT may damp rapid shifts of luminal pH. Enhanced mucosal blood flow plays a significant role in the removal of back-diffusing acid. These neurally coordinated systems act coherently to defend the vulnerable duodenal epithelial cells from concentrated gastric acid.

6

Duodenal mucosal protection by bicarbonate secretion and its mechanisms

58%

Konturek S. J., Konturek P. C., Pawlik T., Sliwowski Z., Ochmanski W., Hahn E. G.

Journal of Physiology and Pharmacology. Supplement

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2004

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tom 55

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nr 2

5-17

Proximal portion of duodenum is exposed to intermittent pulses of gastric H+ discharged by the stomach. This review summarizes the mechanisms of duodenal mucosal integrity, mainly the role of mucus-alkaline secretion and the mucous barrier protecting surface epithelium against gastric H+. The mucous barrier protects the leaky duodenal epithelium against each pulse of gastric H+, which penetrates this barrier and diffuses into duodenocytes, but fails to damage them due to; a) an enhanced expression of cyclooxygenase-1 (COX-1), with release of protective prostaglandins (PG) and of nitric oxide (NO) synthase (NOS) with, however, production of NO, stimulating duodenal HCO3- secretion and b) the release of several neurotransmitters also stimulating HCO3- secretion such as vasoactive intestimal peptide (VIP), pituitary adenylate-cyclase activating polypeptide (PACAP), acetylcholine, melatonin, leptin and ghrelin released by enteric nerves and mucosal cells. At the apical duodenocyte membrane at least two HCO3-/Cl- anion exchangers operate in response to luminal H+ to provide adequate extrusion of HCO3- into duodenal lumen. In the basolateral portion of duodenocyte membrane, both non-electrogenic (NBC) and electrogenic (NBCn) Na+-HCO3- cotransporters are activated by the exposure to duodenal acidification, causing inward movement of HCO3- from extracellular fluid to duodenocytes. There are also at least three Na+/H+ (NHE1-3) amiloride-sensitive exchangers, eliminating H+ which diffused into these cells. The Helicobacter pylori (Hp) infection and gastric metaplasia in the duodenum with bacterium inoculating metaplastic mucosa and inhibiting HCO3- secretion by its endogenous inhibitor, asymetric dimethyl arginine (ADMA), may result in duodenal ulcerogenesis.

Ograniczanie wyników

Adenosine deaminase activity in the human duodenal mucosa in relation to gastric acid secretion

The effect of jejunoectomy on alkaline phosphatase activity in the ileum

Factors influencing the restitution of the duodenal and colonic mucosa after damage

Gastric and duodenal mucosa in children with duodenal ulcer before and after eradication of Helicobacter pylori

Acid-sensing protective mechanisms of duodenum

Duodenal mucosal protection by bicarbonate secretion and its mechanisms