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Effect of multiprobiotic “Symbiter acidophilic” concentrated on morphofunctional changes in stomach evoked by 28-days introduction of omeprazole

100%

Tsyryuk O. I., Beregova T. V.

Journal of Pre-Clinical and Clinical Research

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2010

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tom 04

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nr 1

2

Gastric acid inhibitory profile of ebrotidine, a novel H2-receptor antagonist in humans

100%

Maczka M., Kwiecien N., Obtulowicz W., Konturek S. J., Kaminski K., Oleksy J., Gabryelewicz A., Torres J.

Journal of Physiology and Pharmacology

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1992

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tom 43

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nr 2

This study was designed to assess the gastric secretory effects of ebrotidine, a novel H₂ receptor antagonist, in humans. Three groups (A, В and C) of male subjects with normal gastric mucosa were used. Group A (6 subjects) was used to determine the dose-dependency of gastric inhibitory effect of ebrotidine on basal and pentagastrin- induced maximal acid output. Group В (8 subjects) was employed to examine the duration of the inhibitory effect of ebrotidine on basal and pentagastrin-induced acid secretion. In group C (6 subjects), the 24 h pH-metry was assessed using intraluminal pH-electrode placed in the gastric corpus and connected to a portable recording unit. Single oral dose of ebrotidine (200, 400 or 800 mg) caused a dose- dependent reduction in basal and pentagastrin-induced acid secretion that at a dose of 800 mg amounted to about 89% and 93%, respectively. This inhibition was still observed after 6h and averaged 72% and 50%, respectively. After 12 and 24 h upon the drug intake, both basal and pentagastrin-induced acid secretion returned to the control values. Single oral dose of ebrotidine (800 mg) caused a significant reduction in circadian acidity and resulted in a marked and significant reduction of intragastric acidity for about 6 h upon the administration. This inhibition was accompanied by a transient increase in basal and postprandial gastrin levels. We conclude that ebrotidine is highly effective inhibitor of basal, pentagastrin-induced and circadian gastric acid secretion in humans.

3

New aspects of clinical pharmacology of antacids

100%

Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

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1993

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tom 44

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nr 1

4

Gastric secretion - from Pavlov's NERVISM to Popielski's histamine as direct secretagogue of oxyntic glands

84%

Konturek S. J.

Journal of Physiology and Pharmacology. Supplement

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2003

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tom 54

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nr 3

43-68

Gastric acid and pepsin secretions result from the interplay of neurohormonal factors with stimulatory and inhibitory actions on oxyntic glands. At the turn of XIX century, the notion of nervism or entire neural control of digestive functions, developed by Pavlov prevailed. However, in the second part of XX century, hormonal control has been thought to play a major role in the mechanism of gastric secretion, especially gastrin, which was isolated and synthesized in 1964 by Gregory. Polish traces in gastroenterological history started with the discovery of histamine, a non-nervous and non-gastrin compound in oxyntic mucosa by L. Popielski in 1916, who found that this amine is the most potent and direct stimulant of gastric acid secretion. This histamine concept was supported by leading American gastroenterologists such as A.C. Ivy, championed later by C.F. Code, and clinically applied for testing gastric secretion by K. Kowalewski. Recently, it received a strong support from pharmacological research when J. Black designed H2-receptors antagonists, which were first discovered by M.I. Grossman and S.J. Konturek to inhibit not only histamine-, but also meal- and vagally-induced gastric acid secretion, thus reinforcing the notion of the crucial significance of histamine in the control of gastric secretion as the final common chemostimulator. In conclusion, Polish traces appear to be substantial in gastric history due: 1) to discovery by Popielski that histamine is a major, direct stimulus of gastric secretion; 2) to clinical application of this agent by Kowalewski in testing maximal gastric secretory activity; and 3) to clinical use of histamine H2-antagonists in control of gastric acid secretion and treatment of peptic ulcers.

5

Acid-sensing protective mechanisms of duodenum

67%

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

Wplyw metanolu i jego metabolitow na aktywnosc pepsyny

67%

Dabrowski L., Jasielczuk J., Karwowska A.

Bromatologia i Chemia Toksykologiczna

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2005

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tom 38

|

nr Supl.

357-359

Oceniono wpływ metanolu, formaldehydu i mrówczanu sodu na aktywność preparatu pepsyny i pepsyny występującej w soku żołądkowym.

7

Nitric oxide (NO)-releasing aspirin exhibits a potent esophagoprotection in experimental model of acute reflux esophagitis. Role of nitric oxide and proinflammatory cytokines

67%

Pawlik M., Pajdo R., Kwiecien S., Ptak-Belowska A., Sliwowski Z., Mazurkiewicz-Janik M., Konturek S. J., Pawlik W. W., Brzozowski T.

Journal of Physiology and Pharmacology

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2011

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tom 62

|

nr 1

The purpose of this study was to develop an acute animal model of reflux esophagitis, which would be suitable to induce the esophageal damage caused by gastric acid reflux, thus mimicking the esophageal injury of human gastroesophageal reflux disease (GERD). Global research indicates that GERD is rapidly increasing among the world's population. NSAIDs are known to induce gastrointestinal damage and low doses of aspirin (ASA) have been shown to increase the incidences of GERD in humans. Gastric acid and pepsin secretion and enhanced COX-2 expression were implicated in the pathogenesis of reflux esophagitis, but the effect of selective COX-2 inhibitors against lesions induced by the reflux of gastric acid content into esophagus has not been thoroughly studied. Here, we compared the effect of aspirin (ASA) and so called "safe" nitric oxide (NO) derivative of ASA with those of non-selective and selective cyclooxygenase (COX)-1 and COX-2 in rat model of reflux esophagitis. Reflux esophagitis was induced in anesthetized rats by ligating the pylorus and limiting ridge transitional region between the forestomach and the corpus of stomach. Subsequently, the total gastric reservoir to store gastric juice was greatly diminished, resulting in the reflux of this juice into the esophagus. Rats with esophagitis received intragastric (i.g.) pretreatment either with: 1) vehicle (saline), 2) ASA or NO-ASA (100 mg/kg); 3) the non-selective COX inhibitor, indomethacin (5 mg/kg); 4) the selective COX-1 inhibitor, SC-560 (10 mg/kg), and 5) the selective COX-2 inhibitor, celecoxib (5 mg/kg). In a separate series of rats with reflux oesophagitis, the efficacy of ASA combined with a donor of NO, glyceryl trinitrate (GTN; 10 mg/kg i.g.) to prevent esophageal mucosal injury was investigated. Four hours after induction of esophagitis the gross mucosal damage was graded with a macroscopic lesion index (LI) from 0-6. The esophageal blood flow (EBF) was determined by H2-gas clearance technique, the oesophageal mucosal and blood samples were collected for histology and analysis of the RT-PCR expression and release of proinflammatory cytokines IL-1ß, TNF- and IL-6 using specific ELISA. The exposure of the esophagus to reflux of gastric acid time-dependently increased the esophageal LI and morphologic damage, and decreased EBF with the most significant changes observed at 4 hrs after the ligation procedure. The pretreatment with native ASA in the dose that suppressed the generation of mucosal PGE2, enhanced gross and histologic esophageal damage and produced a significant fall in EBF. NO-ASA or ASA coupled with GTN counteracted the aggravation of the damage and accompanying fall in EBF when compared with native ASA applied alone to rats with esophagitis. The proinflammatory cytokines IL-1ß and TNF- were overexpressed in rats with esophagitis and those pretreated with ASA but this effect was significantly attenuated by NO-ASA. Plasma IL-1ß, TNF- and IL-6 were negligible in the intact rats but significantly increased in those with esophagitis, with this effect being further enhanced by non-selective (indomethacin) and selective (SC-560, celecoxib) COX-1 and COX-2 inhibitors. We conclude that conventional NSAID such as aspirin augments esophagitis, while NO-ASA exerts the beneficial protective effect against reflux esophagitis via the enhancement of esophageal microcirculation due to NO release and an inhibitory effect on expression and release of pro-inflammatory cytokines.

8

Afferent signalling of gastric acid challenge

67%

Holzer P.

Journal of Physiology and Pharmacology. Supplement

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2003

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tom 54

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nr 4

43-53

Gastric acid is a factor in the pain associated with peptic ulcer and other acid-related disorders including functional dyspepsia, given that antisecretory treatment is a mainstay in the treatment of upper abdominal pain. However, the molecular sensors, afferent pathways and central processing systems of gastric chemonociception are little known. This article reviews emerging evidence that vagal afferent pathways play a pivotal role in gastric chemonociception. Exposure of the rat gastric mucosa to backdiffusing concentrations of luminal acid is signalled to the brainstem, but not spinal cord, as visualized by functional neuroanatomy based on the rapid expression of c-fos. This observation is complemented by the finding that the visceromotor response to gastric acid challenge is suppressed by vagotomy, but not splanchnectomy. The gastric acid-induced expression of c-fos in the brainstem is reduced by inhibition of gastric acid secretion and enhanced by pentagastrin-evoked stimulation of gastric acid secretion. These data indicate that endogenous acid modulates the sensory gain of acid-sensitive vagal afferents. Further consistent with a role of these neurons in gastric nociception is the finding that exposure to proinflammatory cytokines and the induction of experimental gastritis or gastric ulceration sensitizes vagal afferent pathways to gastric acid. Taken together, these observations are of relevance to the understanding and treatment of gastric hyperalgesia and dyspeptic pain.

9

Salivary and gastric luminal release of epidermal growth factor under basal conditions and after pentagastrin stimulation in healthy subjects and in duodenal ulcer patients before and after eradication of Helicobacter pylori

67%

Konturek P. C., Ernst H., Konturek J., Bobrzynski A., Kwiecien N., Faller G., Klinger C., Gedliczka O., Hahn E. G.

Journal of Physiology and Pharmacology

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1996

|

tom 47

|

nr 1

10

Helicobacter pylori infection and gastric secretion in duodenal and gastric ulcer patients - the effect of eradication after one year

67%

Laszewicz W., Zaremba-Woroniecka A., Gabryelewicz A.

Journal of Physiology and Pharmacology

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1997

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tom 48

|

nr 3

11

Eradication of Helicobacter pylori and gastrin-somatostatin link in duodenal ulcer patients

67%

Konturek J. W., Bielanski W., Konturek S. J., Domschke W.

Journal of Physiology and Pharmacology

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1996

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tom 47

|

nr 1

12

Stimulation by nitric oxide of gastric acid secretion in bullfrog fundic mucosa in vitro

67%

Kawauchi S., Sugamoto S., Furukawa O., Mimaki H., Takeuchi K.

Journal of Physiology and Pharmacology

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2001

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tom 52

|

nr 1

13

Role of heat shock proteins in gastric inflammation and ulcer healing

59%

Choi S. R., Lee S. A., Kim Y. J., Ok C. Y., Lee H. J., Hahm K. B.

Journal of Physiology and Pharmacology. Supplement

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2009

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tom 60

|

nr 7

14

Brain-gut and appetite regulating hormones in the control of gastric secretion and mucosal protection

59%

Konturek S. J., Brzozowski T., Konturek P. C., Schubert M. L., Pawlik W. W., Padol S., Bayner J.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

|

nr 2

The progress in basic and clinical gastrology indicates that gastric mucosal integrity represents a balance between offensive and defensive factors. The main offensive factors appear to be gastric acid and pepsin under health conditions, while the non-steroidal anti-inflammatory drugs (NSAID) and Helicobacter pylori (H. pylori), infecting this mucosa, are currently considered the most important “aggressive” factors under pathological conditions. To the list of the aggressive factors, also stress, certain cytokines (TNF-, IL-8, IL-11 and IL-18) and oxygen or nitrogen free radicals should be added. The aims of this review is the presentation of the involvement of aggressive and protective factors in the control of gastric acid secretion and appetite regulating hormones in maintaining gastric mucosal integrity and its protection against damaging factors.

15

Helicobacter pylori and impaired gastric secretory functions associated with duodenal ulcer and atrophic gastritis

59%

Konturek P. C., Konturek S. J., Bobrzynski A., Kwiecien N., Obtulowicz W., Stachura J., Hahn E. G., Rembiarz K.

Journal of Physiology and Pharmacology

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1997

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tom 48

|

nr 3

16

Gastric mucosal expression and luminal release of growth factors in gastric carcinoma and duodenal ulcer patients before and after eradication of Helicobacter pylori

59%

Konturek P. C., Bielanski W., Bobrzynski A., Hahn E. G., Konturek S. J.

Journal of Physiology and Pharmacology

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1997

|

tom 48

|

nr 3

17

One week treatment with omeprazole, clarithromycin and tinidazole or lansoprazole, amoxicillin and metronidazole for cure of Helicobacter pylori infection in duodenal ulcer patients

59%

Sito E., Konturek P. C., Bielanski W., Kwiecien N., Konturek S. J., Baniukiewicz A., Jedynak M., Gabryelewicz A., Hahn E. G.

Journal of Physiology and Pharmacology

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1996

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tom 47

|

nr 1

18

Adaptation of gastric mucosa to stress. Effect of ranitidine

59%

Ernst H., Konturek P. C., Brzozowski T., Lochs H., Hahn E. G., Konturek S. J.

Journal of Physiology and Pharmacology

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1998

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tom 49

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nr 3

19

Wlasciwosci pepsyny jako bialka polianionowego. Cz.VII. Kompleksy pepsynogenu z protamina

51%

Roszkowska-Jakimiec W., Jasielczuk J., Gacko M., Worowska A.

Bromatologia i Chemia Toksykologiczna

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2001

|

tom 34

|

nr 1

79-83

Pepsynogen tworzy nierozpuszczalne kompleksy z protaminą. Ilość tych kompleksów zależy od pH środowiska. Kompleksy pepsynogen-protamina rozdysocjowuje chlorek wapnia oraz wysokie stężenie chlorku sodu i mocznika.

20

Gastric secretion and the pathogenesis of peptic ulcer in the Helicobacter pylori infection

51%

Konturek P. C., Konturek J. W., Konturek S. J.

Journal of Physiology and Pharmacology

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1996

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tom 47

|

nr 1

Ograniczanie wyników

Effect of multiprobiotic “Symbiter acidophilic” concentrated on morphofunctional changes in stomach evoked by 28-days introduction of omeprazole

Gastric acid inhibitory profile of ebrotidine, a novel H2-receptor antagonist in humans

New aspects of clinical pharmacology of antacids

Gastric secretion - from Pavlov's NERVISM to Popielski's histamine as direct secretagogue of oxyntic glands

Acid-sensing protective mechanisms of duodenum

Wplyw metanolu i jego metabolitow na aktywnosc pepsyny

Nitric oxide (NO)-releasing aspirin exhibits a potent esophagoprotection in experimental model of acute reflux esophagitis. Role of nitric oxide and proinflammatory cytokines

Afferent signalling of gastric acid challenge

Salivary and gastric luminal release of epidermal growth factor under basal conditions and after pentagastrin stimulation in healthy subjects and in duodenal ulcer patients before and after eradication of Helicobacter pylori

Helicobacter pylori infection and gastric secretion in duodenal and gastric ulcer patients - the effect of eradication after one year

Eradication of Helicobacter pylori and gastrin-somatostatin link in duodenal ulcer patients

Stimulation by nitric oxide of gastric acid secretion in bullfrog fundic mucosa in vitro

Role of heat shock proteins in gastric inflammation and ulcer healing

Brain-gut and appetite regulating hormones in the control of gastric secretion and mucosal protection

Helicobacter pylori and impaired gastric secretory functions associated with duodenal ulcer and atrophic gastritis

Gastric mucosal expression and luminal release of growth factors in gastric carcinoma and duodenal ulcer patients before and after eradication of Helicobacter pylori

One week treatment with omeprazole, clarithromycin and tinidazole or lansoprazole, amoxicillin and metronidazole for cure of Helicobacter pylori infection in duodenal ulcer patients

Adaptation of gastric mucosa to stress. Effect of ranitidine

Wlasciwosci pepsyny jako bialka polianionowego. Cz.VII. Kompleksy pepsynogenu z protamina

Gastric secretion and the pathogenesis of peptic ulcer in the Helicobacter pylori infection