Wyniki wyszukiwania

1

Pharmacological regulation of gastric acid secretion in the apical membrane of parietal cells; a new target for antisecretory drugs

100%

Okabe S., Shimosako K., Amagase K.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 4,1

We examined the local effect of several drugs against secretagogue-stimulated acid secretion in dogs. Test drugs were applied to denervated gastric pouches in conscious dogs either for 5 to 30 min beginning 1 hr after or for 30 min before intravenous infusion of gastric secretagogues (histamine, pentagastrin, or carbachol). The antisecretory effect of test drugs delivered by an intravenous or oral route was also examined. Local application of acid pump inhibitors (omeprazole, leminoprazole) for 30 min beginning l hr after histamine infusion significantly inhibited gastric acid secretion. The effect of leminoprazole persisted for more than 8 hr after a 30 min application. A mast cell stabilizer (FPL 52694) applied to pouches for 15 to 30 min also potently inhibited histamine-stimulated gastric acid secretion in a time-dependent manner. The duration of the antisecretory effect of such drugs after a 30 min application was greater than 4 hr. Locally applied leminoprazole and FPL 52694 for 30 min also significantly inhibited pentagastrin- and carbachol-stimulated gastric acid secretion. Although intravenous omeprazole and leminoprazole exerted a potent antisecretory effect on histamine-induced acid secretion FPL 52694 had little or no antisecretory effect following intravenous or oral administration. 16, 16-dimethyl prostagladin E2 also locally inhibited histamine-stimulated acid secretion. Acid stable local anesthetics (tetracaine, ethyl-4-aminobenzoate), histamine H2-receptor blockers (cimetidine, ranitidine, and famotidine), and a muscarinic M1-receptor antagonist (pirenzepine) did not exhibit local antisecretory effects. Such results strongly suggest that the apical membrane of parietal cells possesses a pharmacologically sensitive portion similar to the basolateral membrane, which usually mediates gastric acid secretion. The apical membrane represents an intriguing target for new antisecretory drugs, as well as a new medium for further elucidating the functional features of parietal cells.

2

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The effect of omeprazole on treatment outcomes in patients with severe traumatic brain injury and sepsis

86%

Oliynyk O.

Health Problems of Civilization

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2021

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tom 15

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nr 2

Background. The interrelation between omeprazole use and the possibility of developing nosocomial pneumonia, acute kidney damage and Clostridium difficile-induced diarrhea in patients with sepsis requires further study. Material and methods. 200 patients with severe craniocerebral injury that underwent surgery for the pathology and developed sepsis in the postoperative period were examined in a blind, randomized placebo-controlled research study. The patients were divided into two groups. Patients in Group 1, as part of their therapy regimen for sepsis, received a daily dose of 0.2 mg/kg omeprazole as an intravenous infusion; patients in Group 2 received placebo instead of omeprazole, in addition to a similar therapy regimen as Group 1. Results. Among patients receiving omeprazole, the number of concomitant ventilatorassociated pneumonia cases increased by 1.32 times, the number of acute kidney damage cases by 1.33 times and the number of cases of Clostridium difficile toxin secretion with feces by 1.75 times. Conclusions. The routine use of omeprazole in the management of patients with sepsis may worsen treatment results.

3

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

86%

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

4

Prostaglandins and ulcer healing

72%

Konturek S. J., Konturek P. C., Brzozowski T.

Journal of Physiology and Pharmacology. Supplement

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2005

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tom 56

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nr 5

5-31

Exogenous prostaglandins (PG) applied in small gastroprotective doses fail to affect healing of gastro-duodenal ulcers but accelerate the healing when used in larger gastric inhibitory doses that appear to enhance COX-2 expression and PGE2 generation in the ulcer area. COX-1 and COX-inhibitors delay ulcer healing, particularly when both COX isoforms are suppressed such e.g. by indomethacin. Dexamethasone, that decreases the expression of COX-2 and mucosal generation of PGE2, delays ulcer healing that can be reversed by the addition of small dose of exogenous PGE2. Proton pump inhibitors (PPI) such as omeprazole and PGE analogs, accelerate ulcer healing mainly due to potent inhibition of gastric acid secretion, but they also augment the COX-2 expression and enzyme activity in the ulcerated mucosa. Endogenous PG generated at ulcer margin appear to be involved in ulcer healing promoted by growth factors and gut hormones such as gastrin or CCK and melatonin acting, at least in part, through increase of induction of COX-2 and local release of PGE2 in the ulcer area . The ulcer healing activity of growth factors (e.g. EGF, TGFalpha, HGF) and certain gut hormones (gastrin, CCK) as well as melatonin, can be attenuated by treatment with COX-1 or COX-2 inhibitors which suppress the release of PGE2 but enhance the expression of COX-2. It is concluded that endogenous PG originating mainly from upregulated COX-2 at the ulcer margin play crucial role in ulcer healing by exogenous PG, PPI, growth factors, gut hormones and melatonin, while COX-1 and COX-2 inhibitors delay ulcer healing by suppressing PG generation, and increasing COX-2 expression in the ulcer area.

5

Inhibition of growth of Helicobacter pylori by omeprazole and clarithromycin enhanced by potassium sorbate

72%

Popowski J., Grodowska A., Kafel S.

Journal of Physiology and Pharmacology. Supplement

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1997

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tom 48

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nr 1

6

Involvement of heat shock proteins in the healing of acetic acid-induced gastric ulcers in rats

72%

Tsukimi Y., Nakai H., Itoh S., Amagase K., Okabe S.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 3

7

Therapy of Helicobacter pylori infection

72%

Bazzoli F.

Journal of Physiology and Pharmacology. Supplement

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1997

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tom 48

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nr 1

8

Evaluation of omeprazole and amoxicillin or omeprazole and clarithromycin treatment in children with Helicobacter pylori gastritis or duodenal ulcer disease

72%

Iwanczak F., Potyrala M., Iwanczak B., Gosciniak G.

Journal of Physiology and Pharmacology. Supplement

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1997

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tom 48

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nr 1

9

Multicenter evaluation of dual-therapy [omeprazole and amoxicillin] for Helicobacter pylori-associated duodenal and gastric ulcer [two years of the observation]

72%

Gabryelewicz A., Laszewicz W., Dzieniszewski J., Ciok J., Marlicz K., Bielicki D., Popiela T., Knapik Z., Poniewierka E.

Journal of Physiology and Pharmacology. Supplement

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1997

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tom 48

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nr 1

10

Omeprazole fails to suppress up-regulation of gastric mucosal endothelin-converting enzyme-1 by Helicobacter pylori lipopolysaccharide

72%

Slomiany B. L., Piotrowski J., Slomiany A.

Journal of Physiology and Pharmacology

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2000

|

tom 51

|

nr 3

11

Multicenter evaluation of dual-therapy [omeprazol and amoxycillin] for Helicobacter pylori-associated duodenal and gastric ulcer. [Two years of the observation]

72%

Gabryelewicz A., Laszewicz W., Dzieniszewski J., Ciok J., Marlicz K., Bielecki D., Popiela T., Legutko J., Knapik Z., Poniewierka E.

Journal of Physiology and Pharmacology. Supplement

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1997

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tom 48

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nr 4

12

Targeting the fungal plasma membrane proton pump

72%

Monk B. C., Mason A. B., Kardos T. B., Perlin D. S.

Acta Biochimica Polonica

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1995

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tom 42

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nr 4

The need for new mechanistic classes of broad spectrum antifungal agents has prompted development of the membrane sector and ectodomain of the plasma membrane proton pumping ATPase as an antifungal target. The fungal proton pump is a highly abundant, essential enzyme in Saccharomyces cerevisiae. It belongs to the family of P-type ATPases, a class of enzymes that includes the Na+,K+-ATPase and the gastric H+,K+-ATPase. These enzymes are cell surface therapeutic targets for the cardiac glycosides and several anti-ulcer drugs, respectively. The effects of acid- -activated omeprazole show that extensive inhibition of the S. cerevisiae ATPase is fungicidal. Fungal proton pumps possess elements within their transmembrane loops that distinguish them from other P-type ATPases. These loops, such as the conformationally sensitive transmembrane loop 1+2, can attenuate the activity of the enzyme. Expression in S. cerevisiae of fully functional chimeric ATPases that contain a foreign target comprising transmembrane loops 1+2 and/or 3+4 from the fungal pathogen Candida albicans suggests that these loops operate as a domain. The chimera containing C. albicans transmembrane loops 1+2 and 3+4 provides a prototype for mutational analysis of the target region and the screening of inhibitors directed against opportunistic fungal pathogens. Panels of mutants with modified ATPase regulation or with altered cell surface cysteine residues are also described. Information about the ATPase membrane sector and ectodomain has been integrated into a model of this region.

13

Prevention and treatment of ulcers induced by nonsteroidal anti-inflammatory drugs: an update

58%

Dajani E. Z., Agrawal N. M.

Journal of Physiology and Pharmacology

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1995

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tom 46

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nr 1

14

Future treatment of peptic ulcer: is there room for anti-infective drugs?

58%

Dajani E. Z.

Journal of Physiology and Pharmacology

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1993

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tom 44

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nr 1

15

Up-regulation of endothelin-1 in gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide: effect of omeprazole and sucralfate

58%

Slomiany B. L., Piotrowski J., Slomiany A.

Journal of Physiology and Pharmacology

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2000

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tom 51

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nr 2

16

A new ulcer model unhealed gastric ulcers, induced by chronic treatment with indomethacin in rats with acetic acid ulcers

58%

Amagase K., Okabe S.

Journal of Physiology and Pharmacology

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1999

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tom 50

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nr 2

17

Temporary elevation of pancreatic lysosomal enzymes, as a result of the omeprazole-induced peripancreatic inflammation in male Wistar rats

58%

Burdan F., Siezieniewska Z., Maciejewski R., Burski K., Wojtowicz Z.

Journal of Physiology and Pharmacology

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2000

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tom 51

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nr 3

18

The reinfection of H.pylori two years after quadruple therapy for duodenal ulcer

58%

Bobrzynski A., Budzynski A., Bielanski W., Kaminska A., Gedliczka O., Konturek S. J., Stachura J.

Journal of Physiology and Pharmacology. Supplement

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1997

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tom 48

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nr 1

19

Strategies for Helicobacter pylori eradication in 1995: A review of international and Belgian experience

58%

Deltenre M., Jonas C., Otero J., Cozzoli A., Denis P., Burette A., De Koster E.

Journal of Physiology and Pharmacology

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1996

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tom 47

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nr 1

20

Effects of melatonin and tryptophan on healing of gastric and duodenal ulcers with Helicobacter pylori infection in humans

51%

Celinski K., Konturek P. C., Konturek S. J., Slomka M., Cichoz-Lach H., Brzozowski T., Bielanski W.

Journal of Physiology and Pharmacology

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2011

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tom 62

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nr 5

Ograniczanie wyników

Pharmacological regulation of gastric acid secretion in the apical membrane of parietal cells; a new target for antisecretory drugs

The effect of omeprazole on treatment outcomes in patients with severe traumatic brain injury and sepsis

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

Prostaglandins and ulcer healing

Inhibition of growth of Helicobacter pylori by omeprazole and clarithromycin enhanced by potassium sorbate

Involvement of heat shock proteins in the healing of acetic acid-induced gastric ulcers in rats

Therapy of Helicobacter pylori infection

Evaluation of omeprazole and amoxicillin or omeprazole and clarithromycin treatment in children with Helicobacter pylori gastritis or duodenal ulcer disease

Multicenter evaluation of dual-therapy [omeprazole and amoxicillin] for Helicobacter pylori-associated duodenal and gastric ulcer [two years of the observation]

Omeprazole fails to suppress up-regulation of gastric mucosal endothelin-converting enzyme-1 by Helicobacter pylori lipopolysaccharide

Multicenter evaluation of dual-therapy [omeprazol and amoxycillin] for Helicobacter pylori-associated duodenal and gastric ulcer. [Two years of the observation]

Targeting the fungal plasma membrane proton pump

Prevention and treatment of ulcers induced by nonsteroidal anti-inflammatory drugs: an update

Future treatment of peptic ulcer: is there room for anti-infective drugs?

Up-regulation of endothelin-1 in gastric mucosal inflammatory responses to Helicobacter pylori lipopolysaccharide: effect of omeprazole and sucralfate

A new ulcer model unhealed gastric ulcers, induced by chronic treatment with indomethacin in rats with acetic acid ulcers

Temporary elevation of pancreatic lysosomal enzymes, as a result of the omeprazole-induced peripancreatic inflammation in male Wistar rats

The reinfection of H.pylori two years after quadruple therapy for duodenal ulcer

Strategies for Helicobacter pylori eradication in 1995: A review of international and Belgian experience

Effects of melatonin and tryptophan on healing of gastric and duodenal ulcers with Helicobacter pylori infection in humans