Wyniki wyszukiwania

1

The animal model of acute pancreatitis induced by synthetic prooxidant

100%

Sledzinski Z., Wozniak M., Brunelli A., Scutti G., Stanek A., Bertoli E., Lezoche E., Wajda Z.

Polish Journal of Environmental Studies

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1998

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tom 07

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nr 6

2

Parenteral nutrition with lipids in multiple organ failure complicating acute pancreatitis

88%

Wojcik Z., Pertkiewicz M., Szczygiel B.

Journal of Physiology and Pharmacology. Supplement

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1998

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tom 49

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nr 2

3

Does ERCP have a role in the treatment of severe acute pancreatitis?

88%

Folsch U. R.

Journal of Physiology and Pharmacology. Supplement

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1998

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tom 49

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nr 2

4

Functional and morphological recovery after acute necrotizing pancreatitis

88%

Niederau C.

Journal of Physiology and Pharmacology. Supplement

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1998

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tom 49

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nr 2

5

Protective and therapeutic effect of heparin in acute pancreatitis

75%

Ceranowicz P., Dembinski A., Warzecha Z., Dembinski M., Cieszkowski J., Rembiasz K., Konturek S. J., Kusnierz-Cabala B., Tomaszewska R., Pawlik W. W.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

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nr 4

103-125

6

Administration of warfarin accelerates the recovery in ischemia/reperfusion-induced acute pancreatitis

75%

Maduzia D., Ceranowicz P., Cieszkowski J., Chmura A., Galazka K., Kusnierz-Cabala B., Warzecha Z.

Journal of Physiology and Pharmacology

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2020

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tom 71

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nr 3

7

Nesfatin-1 protects from acute pancreatitis: role of melanocortin receptors

75%

Buzcu H., Ozbeyli D., Yuksel M., Cilingier Kaya O. T., Kasimay Cakir O.

Journal of Physiology and Pharmacology

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2019

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tom 70

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nr 6

8

Effects of adenosine receptor agonists and antagonists on cytochrome P450 extinction in the liver of rats in the course of acute pancreatitis

75%

Celinski K., Madro A., Czechowska G., Slomka M., Prozorow-Krol B., Biskup W., Malm A., Juda M., Wielosz M.

Medycyna Weterynaryjna

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2007

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tom 63

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nr 05

528-531

In the course of acute pancreatitis the liver is an organ that is especially exposed to damage. The presence of adenosine receptors was observed in the whole digestive system. The aim of the experiment was to define the correlation between the extinction of cytochrome P450 in the liver of rats and adenosine receptor agonists and antagonists in the course of necrotizing acute pancreatitis. The experiments were carried out on Wistar male rats weighing 250 g. Acute pancreatitis was induced injecting 5% sodium taurocholate to the biliary-pancreatic duct. Prior to the induction of acute pancreatitis the animals were injected intraperitoneally with selective agonists and antagonists: CGS 21680 (selective A2 agonist), 3 mg/kg, ZM 241385 (selective A2a antagonist), 3 mg/kg, DPCPX (A1 antagonist), 1 mg/kg, 1.3-Dipropyl-8-phenylxantine (selective A1 antagonist), 3 mg/kg, IB-MECA (A3 agonist), 0.75 mg/kg. The determinations were performed in hepatic microsomes obtained according to Guegenrichs method Cytochrome P450 extinction was determined by Matsubars technique. The results obtained reveal statistically significantly decreased cytochrome P450 extinction after sodium taurocholate administration. Decreased levels of extinction were also observed after combined administration of sodium taurocholate + Phenylxantine and sodium taurocholate + ZM. The level of IB-MECA remained unchanged in comparison to the controls. However DPCPX and CGS administration increased the extinction of cytochrome P450. The diverse influence of adenosine receptor agonists and antagonists used in the experiment on cytochrom P450 extinction seems to modify the course of the inflammatory process after using 5% sodium taurocholate.

9

Effect of sensory nerves and CGRP on the development of caerulein-induced pancreatitis and pancreatic recovery

75%

Warzecha Z., Dembinski A., Ceranowicz P., Stachura J., Tomaszewska R., Konturek S. J.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 4,1

The function of primary sensory neurons is to receive and transmit information from external environment and these neurons are able to release neuromediators from the activated peripheral endings. The aim of this study was to determine the influence of sensory nerves and administration of their mediator — calcitonin gene related peptide (CGRP) on the course of acute pancreatitis (AP). Ablation of sensory nerves was performed by neurotoxic dose of capsaicin (100 mg/kg). Single or repeated episodes of AP were induced by caerulein infusion (10 µg/kg/h for 5 h). Five repeated AP were performed once a week. Capsaicin at the dose which stimulates sensory nerves (0.5 mg/kg/dose) or CGRP (10 µg/kg/dose) was administrated before and during or after single induction of AP, as well as, after each induction of repeated AP. Rats were killed at the time 0, 3 or 9 h after single induction of AP or two weeks after last induction of repeated AP. Ablation of sensory nerves aggravated pancreatic damage in caerulein-induced AP. Treatment with stimulatory doses of capsaicin or CGRP before and during single induction of AP attenuated the pancreatic damage in morphological examination. This effect was also manifested by partial reversion of AP evoked drop in DNA synthesis and pancreatic blood flow (PBF). Administration of CGRP after single AP induction aggravated histologically manifested pancreatic damage. The further decrease in PBF and DNA synthesis was also observed. Animals with five episodes of AP showed almost full pancreatic recovery two weeks after last induction of AP concerning all parameters tested. In stimulatory doses of capsaicin treated rats, we observed the decrease in pancreatic amylase and fecal chymotrypsin activity, as well as, the drop in DNA synthesis. Similar but less pronounced effects were observed after treatment with CGRP. We conclude that effect of sensory nerves and CGRP on AP is two-phase and time dependent. Stimulation of sensory nerves or the administration of CGRP during development of AP exhibits protective effects against pancreatic damage induced by caerulein overstimulation. After induction of AP, persistent activity of sensory nerves and presence of CGRP aggravate pancreatic damage and lead to functional insufficiency typical for chronic pancreatitis.

10

Residual changes of morphology and function of pancreas after the first attack of acute pancreatitis

75%

Dite P., Zboril V., Novotny I., Munzova H., Hep A., Kunovska M., Precechtelova M.

Journal of Physiology and Pharmacology. Supplement

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1998

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tom 49

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nr 2

11

The pathogenesis and pathophysiology of acute pancreatitis

75%

Steer M. L.

Journal of Physiology and Pharmacology. Supplement

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1998

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tom 49

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nr 2

12

Does chronic ethanol administration have influence on pancreatic regeneration in the course of caerulein induced acute pancreatitis in rats

75%

Rydzewska G., Jurkowska G., Dzieciol J., Faszczewska A., Wroblewski E., Gabryelewicz A.

Journal of Physiology and Pharmacology

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2001

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tom 52

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nr 4,2

This study was undertaken in order to determine the influence of chronic ethanol administration on pancreatic regeneration during acute pancreatitis (AP). Rats were pair fed with isocaloric diet containing or not ethanol. After 8 weeks of such feeding AP was induced by sc injection of caerulein (Cae). 6 h, 24 h and 5 days after first Cae dose pancreatic weight, amylase, chymotrypsin, protein, RNA, DNA contents were determined and phosphatidic acid (PA) production in isolated pancreatic acini was measured. Proliferating cells were quantified by immunochemical staining of cells incorporating bromodeoxyuridine (BrdU). Results: Pancreatic weight was significantly higher at 6 h after first Cae injection in both, ethanol fed (EF) and control groups (C), however at 24 h pancreatic weight did not differ from prior to AP induction in EF rats. Ethanol feeding (EF) did not influence significantly protein, chymotrypsin and amylase content in pancreatic tissue in groups with AP. In EF rats RNA content after 5 days of AP was higher than in control animals. Total DNA content in EF rats with AP was lower 6 h after AP induction, earlier than in control animals with AP. Immunochemistry showed higher labelling index for BrdU after 6 h, 24 h and 5 days of AP in EF rats. In contrast to this findings, in EF animals, AP induction was not able to stimulate further PA accumulation. Conclusion: We conclude that chronic ethanol feeding, while inhibiting PA accumulation in comparison to control group, does not impair pancreatic tissue regeneration during the early phase of Cae-induced AP. Stimulation of regenerative/reparative processes in EF rats during Cae-induced AP seems to be even more pronounced than in the control group.

13

The role of phospholipases A2 in the pathophysiology of acute pancreatitis. A review

75%

Hietaranta A. J., Kemppainen E. A., Gronroos J. M., Nevalainen T. J.

Journal of Physiology and Pharmacology. Supplement

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1998

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tom 49

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nr 2

14

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The effect of nafamostat mesilate [FUT-175] and gabexate mesilate [FOY] on multiorgan oxidant-antioxidant balance in acute experimental pancreatitis

75%

Dabrowski A., Gabryelewicz A.

Journal of Physiology and Pharmacology

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1994

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tom 45

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nr 3

15

Ghrelin attenuates the development of acute pancreatitis in rats

75%

Dembinski A., Warzecha Z., Ceranowicz P., Tomaszewska R., Stachura J., Konturek S. J., Konturek P. C.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 4

Ghrelin, a circulating growth hormone-releasing peptide isolated from human and rat stomach, stimulates growth hormone secretion, food intake and exhibits gastroprotective properties. Ghrelin is predominantly produced by a population of endocrine cells in the gastric mucosa, but its presence in bowel, pancreas, pituitary and hypothalamus has been reported. In human fetal pancreas, ghrelin is expressed in a prominent endocrine cell population. In adult pancreatic islets the population of these cell is reduced. The aim of present study was to investigate the influence of ghrelin administration on the development of acute pancreatitis. Methods: Acute pancreatitis was induced in rat by caerulein injection. Ghrelin was administrated twice (30 min prior to the first caerulein or saline injection and 3 h later) at the doses: 2, 10 or 20 nmol/kg. Immediately after cessation of caerulein or saline injections the following parameters were measured: pancreatic blood flow, plasma lipase activity, plasma interleukin-1ß (IL-1ß) and interleukin 10 (IL-10) concentration, pancreatic DNA synthesis, and morphological signs of pancreatitis. Results: Administration of ghrelin without induction of pancreatitis did not affect significantly any parameter tested. Caerulein led to the development of acute edematous pancreatitis. Treatment with ghrelin at the dose 2 nmol/kg, during induction of pancreatitis, was without effect on pancreatic histology or biochemical and functional parameters. Treatment with ghrelin at the dose 10 and 20 nmol/kg attenuated the development of pancreatitis and the effects of both doses were similar. Administration of ghrelin (10 or 20 nmol/kg) reduced inflammatory infiltration of pancreatic tissue and vacuolization of acinar cells. Also, plasma lipase activity and plasma IL-1ß concentration were reduced, and caerulein-induced fall in pancreatic DNA synthesis was reversed. Administration of ghrelin at the dose 10 and 20 nmol/kg was without effect on caerulein-induced pancreatic edema and pancreatitis-related fall in pancreatic blood flow. Conclusions: (1) Administration of ghrelin attenuates pancreatic damage in caerulein-induced pancreatitis; (2) Protective effect of ghrelin administration seems to be related the inhibition in inflammatory process and the reduction in liberation of pro-inflammatory IL-1ß.

16

Peritoneal lavage in acute pancreatitis

75%

Krawczyk M., Plaszczyk D., Paczkowski P. M., Najnigier B., Zieniewicz K., Patkowski W., Gackowski W., Karwowski A.

Journal of Physiology and Pharmacology. Supplement

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1998

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tom 49

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nr 2

17

Platelet activating factor [PAF] inhibitor [TCV-309] reduces caerulein - and PAF-induced pancreatitis. A morphologic and functional study in the rat

75%

Tomaszewska R., Dembinski A., Warzecha Z., Banas M., Konturek S. J., Stachura J.

Journal of Physiology and Pharmacology

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1992

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tom 43

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nr 4

Caerulein-induced acute pancreatitis was studied in rats. Consistent with this type of acute pancreatitis morphological (edema, leukocytic infiltration and acinar cell vaculization) and biochemical (increase in pancreatic protein content, PAF release and serum amylase) changes developed 5 hours after caerulein administration. In addition increase in pancreatic weight and decrease in pancreatic blood flow were noticed. PAF administration caused pancreatic damage similar in some parameters to caerulein-induced pancreatitis, along with reduction of pancreatic blood flow, increase in pancreatic protein content, and serum amylase. TCV-309, a selective PAF antagonist, administered prior to caerulein and/or PAF, reduced caerulein-induced pancreatitis and prevented PAF-induced pancreatitis. Results of our present studies indicate the crucial role of PAF in pathogenesis of experimental acute pancreatitis.

18

IGF-1 stimulates production of interleukin-10 and inhibits development of caerulein-induced pancreatitis

75%

Warzecha Z., Dembinski A., Ceranowicz P., Konturek S. J., Tomaszewska R., Stachura J., Konturek P. C.

Journal of Physiology and Pharmacology

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2003

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tom 54

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nr 4

Insulin-like growth factor-1 (IGF-1) and other growth factors overexpression was reported in acute pancreatitis. Previous studies have shown the protective effect of epidermal growth factor (EGF), Hepatocyte Growth Factor (HGF) and Fibroblast Growth Factor (FGF) in the course of experimental acute pancreatitis. The aim of our studies was to determine the effect of IGF-1 administration on the development of caerulein-induced pancreatitis. Methods: Acute pancreatitis was induced by infusion of caerulein (10 µg/kg/h) for 5 h. IGF-1 was administrated twice at the doses: 2, 10, 50, or 100 µg/kg s.c. Results: Administration of IGF-1 without induction of pancreatitis increased plasma interleukin-10 (IL-10). Infusion of caerulein led to development of acute edematous pancreatitis. Histological examination showed pancreatic edema, leukocyte infiltration and vacuolization of acinar cells. Also, acute pancreatitis led to an increase in plasma lipase and interleukin 1ß (IL-1ß) level, whereas pancreatic DNA synthesis and pancreatic blood flow were decreased. Treatment with IGF-1, during induction of pancreatitis, increased plasma IL-10 and attenuated the pancreatic damage, what was manifested by histological improvement of pancreatic integrity, the partial reversion of the drop in pancreatic DNA synthesis and pancreatic blood flow, and the reduction in pancreatitis-evoked increase in plasma amylase, lipase and IL-1ß level. Protective effect of IGF-1 administration was dose-dependent. Similar strong protective effect was observed after IGF-1 at the dose 2 x 50 and 2 x 100 µg/kg. Conclusions: (1) Administration of IGF-1 attenuates pancreatic damage in caerulein-induced pancreatitis; (2) This effect is related, at least in part, to the increase in IL-10 production, the reduction in liberation of IL-1ß and the improvement of pancreatic blood flow.

19

Protective role of endogenous nitric oxide (NO) in lipopolysaccharide - induced pancreatic damage. (A new experimental model of acute pancreatitis)

75%

Jaworek J., Jachimczak B., Bonior J., Kot M., Tomaszewska R., Karczewska E., Stachura J., Pawlik W., Konturek S. J.

Journal of Physiology and Pharmacology

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2000

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tom 51

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nr 1

20

Hepatic complications in acute pancreatitis

75%

Dlugosz J. W.

Journal of Physiology and Pharmacology. Supplement

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1998

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tom 49

|

nr 2

Ograniczanie wyników

The animal model of acute pancreatitis induced by synthetic prooxidant

Parenteral nutrition with lipids in multiple organ failure complicating acute pancreatitis

Does ERCP have a role in the treatment of severe acute pancreatitis?

Functional and morphological recovery after acute necrotizing pancreatitis

Protective and therapeutic effect of heparin in acute pancreatitis

Administration of warfarin accelerates the recovery in ischemia/reperfusion-induced acute pancreatitis

Nesfatin-1 protects from acute pancreatitis: role of melanocortin receptors

Effects of adenosine receptor agonists and antagonists on cytochrome P450 extinction in the liver of rats in the course of acute pancreatitis

Effect of sensory nerves and CGRP on the development of caerulein-induced pancreatitis and pancreatic recovery

Residual changes of morphology and function of pancreas after the first attack of acute pancreatitis

The pathogenesis and pathophysiology of acute pancreatitis

Does chronic ethanol administration have influence on pancreatic regeneration in the course of caerulein induced acute pancreatitis in rats

The role of phospholipases A2 in the pathophysiology of acute pancreatitis. A review

The effect of nafamostat mesilate [FUT-175] and gabexate mesilate [FOY] on multiorgan oxidant-antioxidant balance in acute experimental pancreatitis