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1
Content available remote

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

100%
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
2
Content available remote

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

100%
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.
3
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Pretreatment with low doses of acenocoumarol inhibits the development of acute ischemia/reperfusion-induced pancreatitis

84%
Warzecha Z., Sendur P., Ceranowicz P., Dembinski M., Cieszkowski J., Kusnierz-Cabala B., Tomaszewska R., Dembinski A.
Journal of Physiology and Pharmacology
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2015
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tom 66
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nr 5
4
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Heparin inhibits protective effect of ischemic preconditioning in ischemia/reperfusion-induced acute pancreatitis

84%
Warzecha Z., Dembinski A., Ceranowicz P., Dembinski M., Sendur R., Cieszkowski J., Sendur P., Tomaszewska R.
Journal of Physiology and Pharmacology
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2012
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tom 63
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nr 4
5
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Influence of ischemic preconditioning on blood coagulation, fibrinolytic activity and pancreatic repair in the course of caerulein-induced acute pancreatitis in rats

84%
Warzecha Z., Dembinski A., Ceranowicz P., Dembinski M., Cieszkowski J., Kusnierz-Cabala B., Naskalski J. W., Jaworek J., Konturek S. J., Pawlik W. W., Tomaszewska R.
Journal of Physiology and Pharmacology
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2007
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tom 58
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nr 2
Previous studies have shown that ischemic preconditioning protects several organs, including the pancreas, from ischemia/reperfusion-induced injury. The aim of the investigation was to determine whether ischemic preconditioning affects the course edematous pancreatitis. Methods: In rats, ischemic preconditioning was performed by short-term clamping the celiac artery. Acute pancreatitis was induced by caerulein. The severity of acute pancreatitis was evaluated between the first and tenth day of inflammation. Results: Ischemic preconditioning applied alone caused a mild pancreatic damage. Combination of ischemic preconditioning with caerulein attenuated the severity of pancreatitis in histological examination and reduced the pancreatitis-evoked increase in plasma lipase and pro-inflammatory interleukin-1ß. This effect was associated with an increase in plasma level of anti-inflammatory interleukin-10 and partial reversion of the pancreatitis-evoked drop in pancreatic DNA synthesis and pancreatic blood flow. In secretory studies, ischemic preconditioning in combination with induction of acute pancreatitis attenuated the pancreatitis-evoked decrease in secretory reactivity of isolated pancreatic acini to stimulation by caerulein. In the initial period of acute pancreatitis, ischemic preconditioning alone and in combination with caerulein-induced acute pancreatitis prolonged the activated partial thromboplastin time (APTT), increased plasma level of D-dimer and shortened the euglobulin clot lysis time. The protective effect of ischemic preconditioning was observed during entire time of experiment and led to acceleration of pancreatic regeneration. Conclusions: Ischemic preconditioning reduces the severity of caerulein-induced pancreatitis and accelerates pancreatic repair; and this effect is related to the activation of fibrinolysis and reduction of inflammatory process.
6
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Role of endogenous melatonin and its MT2 receptor in the modulation of caerulein-induced pancreatitis in the rat

84%
Jaworek J., Konturek S. J., Leja-Szpak A., Nawrot K., Bonior J., Tomaszewska R., Stachura J., Pawlik W. W.
Journal of Physiology and Pharmacology
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2002
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tom 53
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nr 4,2
The present study investigated the involvement of endogenous melatonin in the prevention of pancreatic damage provoked by caerulein-induced pancreatitis (CIP) by using the luzindole, the antagonist of melatonin MT2 receptors. CIP was produced by subcutaneous infusion of caerulein to conscious rats (25 µg/kg). Luzindole (1, 2 or 4 mg/kg) was given as an intraperitoneal bolus injection 30 min prior to the start of CIP. Lipid peroxidation products, malondialdehyde (MDA) and 4- hydroxynonenal (4-HNE) were measured in the pancreas by LPO-584 commercial kit. CIP was confirmed by histological examination and manifested by significant increases of plasma activities of amylase, lipase and tumor necrosis factor a (TNFalpha) (by 500%, 1000% and 600%, respectively) comparing to the control values. This was accompanied by a 40% limitation in pancreatic blood flow (PBF) and by 200% increase of MDA+4-HNE in the pancreas of CIP rats. Administration of luzindole to the CIP rats reduced PBF, aggravated the histological manifestations of pancreatitis, resulted in the significant augmentation of pancreatic MDA + 4-HNE content, and produced the marked increases of plasma levels of lipase, amylase and TNFalpha, comparing to the values observes in the rats with CIP alone. These results suggest that endogenous melatonin through its receptor MT2 plays an important role in the attenuation of pancreatic damage produced by overstimulation with caerulein.
7
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Influence of leptin administration on the course of acute ischemic pancreatitis

84%
Warzecha Z., Dembinski A., Ceranowicz P., Jaworek J., Konturek P. C., Dembinski M., Bilski J., Konturek S. J.
Journal of Physiology and Pharmacology
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2002
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tom 53
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nr 4,2
Leptin is involved in the regulation of food intake and previous studies have shown that leptin affects the inflammatory response in various tissues. The objective of this study was to examine the influence of leptin administration on the development and the course of acute ischemic pancreatitis. Acute pancreatitis was induced by limitation of pancreatic blood flow by clamping of inferior splenic artery for 30 min, followed by reperfusion. Leptin was administered three times daily at the dose 10 or 50 µg/kg. Animals were sacrificed 1, 3, 5, 10 and 21 days after removal of vascular clips. Administration of leptin reduced development of pancreatic damage and accelerated pancreatic regeneration what was manifested by the improvement of pancreatic histology, the decrease in serum lipase and amylase activity, and the reduction in serum interleukin-1ß concentration. Also, treatment with leptin caused the increase in the pancreatic blood flow and pancreatic DNA synthesis. Leptin administration was without effect on serum interleukin-10 concentration. Leptin at the dose 50 µg/kg was more effective than 10 µg/kg. We conclude that leptin reduces the pancreatic damage in the course of ischemic pancreatitis and accelerates the pancreatic tissue repair. The beneficial effects of leptin appear to be dependent on the improvement of pancreatic blood flow, the increase in pancreatic cell growth, and the limitation of pro-inflammatory interleukin-1ß release.
8
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Content available

Pancreatic damage and regeneration in the course of ischemia-reperfusion induced pancreatitis in rats

84%
Dembinski A., Warzecha Z., Ceranowicz P., Stachura J., Tomaszewska R., Konturek S. J., Sendur R., Dembinski M., Pawlik W. W.
Journal of Physiology and Pharmacology
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2001
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tom 52
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nr 2
9
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The effect of exogenous apelin on the secretion of pancreatic juice in anaesthetized rats

67%
Kapica M., Jankowska A., Antushevich H., Pietrzak P., Bierla J. B., Dembinski A., Zabielski R.
Journal of Physiology and Pharmacology
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2012
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tom 63
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nr 1
10
Content available remote

Pretreatment with obestatin inhibits the development of cerulein-induced pancreatitis

67%
Ceranowicz P., Warzecha Z., Dembinski A., Cieszkowski J., Dembinski M., Sendur R., Kusnierz-Cabala B., Tomaszewska R., Kuwahara A., Kato I.
Journal of Physiology and Pharmacology
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2009
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tom 60
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nr 3
95-101
Obestatin is a peptide derived from the proghrelin, a common prohormone for ghrelin and obestatin. Obestatin, like the ghrelin has been originally extracted from rat stomach, and the stomach seems to be a major source of circulating obestatin. Previous studies have shown that administration of ghrelin exhibits protective effect in the pancreas, inhibiting the development of acute pancreatitis. Recent study has shown that obestatin promotes survival of ß-cells and pancreatic islets. Aim of the present study was to investigate the influence of obestatin administration on the development of cerulein-induced pancreatitis. Studies were performed on male Wistar rats. Acute pancreatitis was induced by cerulein given intraperitoneally 5 times at a dose of 50 µg/kg/dose with 1-h intervals. Obestatin was injected twice intraperitoneally at the dose of 4, 8 or 16 nmol/kg/dose. In control saline-treated rats, obestatin was without effect on pancreatic morphology, serum activity of pancreatic enzymes, serum level of pro-inflammatory interleukin-1b or pancreatic cells proliferation. In animals with induction of acute pancreatitis, morphological examination showed that administration of obestatin decreased pancreatic leukocyte infiltration and vacuolization of acinar cells. These effects were accompanied by reduction in the pancreatitis-evoked increase in serum level of pancreatic digestive enzymes, lipase amylase and poly-C ribonuclease. Obestatin administered at the highest dose of 16 nmo/kg/dose reduced serum activity of these enzymes by 33, 42 and 44%, respectively. Also serum concentration of pro-inflammatory interleukin-1ß was decreased by obestatin in rats with acute pancreatitis; whereas the pancreatitis-evoked decrease in pancreatic blood flow and pancreatic DNA synthesis was partially reversed. Administration of obestatin reduces the severity of cerulein-induced acute pancreatitis. This effect is related, at least in part, to the improvement of pancreatic blood flow and reduction in pro-inflammatory interleukin-1ß release.
11
Content available remote

Therapeutic effect of ghrelin in the course of cerulein-induced acute pancreatitis in rats

67%
Warzecha Z., Ceranowicz P., Dembinski A., Cieszkowski J., Kusnierz-Cabala B., Tomaszewska R., Kuwahara A., Kato I.
Journal of Physiology and Pharmacology
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2010
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tom 61
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nr 4
419-427
Recent studies have shown that pretreatment with ghrelin exhibits protective effect in the gut. Administration of ghrelin reduces gastric mucosal damage, as well as inhibits the development of experimental pancreatitis. However, this protective effect requires administration of ghrelin before gastric or pancreatic damage and thus has a limited clinical value. The aim of present study was to assess the influence of ghrelin administered after development of acute pancreatitis on the course of this disease. Acute pancreatitis was induced by cerulein. Ghrelin was administered twice a day for 1, 2, 4, 6 or 9 days at the dose of 4, 8 or 16 nmol/kg/dose. The first dose of ghrelin was given 24 hours after last injection of cerulein. The severity of acute pancreatitis was assessed between 0 h and 10 days after cessation of cerulein administration. Administration of caerulein led to the development of acute edematous pancreatitis and maximal severity of this disease was observed 24 hours after induction of pancreatitis. Treatment with ghrelin reduced morphological signs of pancreatic damage such as pancreatic edema, leukocyte infiltration and vacuolization of acinar cells, and led to earlier regeneration of the pancreas. Also biochemical indexes of the severity of acute pancreatitis, serum activity of lipase and amylase were significantly reduced in animals treated with ghrelin. These effects were accompanied by an increase in the pancreatic DNA synthesis and a decrease in serum level of pro-inflammatory interleukin-1ß. Administration of ghrelin improved pancreatic blood flow in rats with acute pancreatitis. We conclude that: (1) treatment with ghrelin exhibits therapeutic effect in caerulein-induced experimental acute pancreatitis; (2) this effect is related, at least in part, to the improvement of pancreatic blood flow, reduction in proinflammatory interleukin-1b and stimulation of pancreatic cell proliferation.
12
Content available remote

Extract of grapefruit-seed reduces acute pancreatitis induced by ischemia-reperfusion in rats; possible implication of tissue antioxidants

67%
Dembinski A., Warzecha Z., Konturek S. J., Ceranowicz P., Dembinski M., Pawlik W. W., Kusnierz-Cabala B., Naskalski J. W.
Journal of Physiology and Pharmacology
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2004
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tom 55
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nr 4
Grapefruit seed extract (GSE) has been shown to exert antibacterial, antifungal and antioxidant activity possibly due to the presence of naringenin, the flavonoid with cytoprotective action on the gastric mucosa. No study so far has been undertaken to determine whether this GSE is also capable of preventing acute pancreatic damage induced by ischemia/reperfusion (I/R), which is known to result from reduction of anti-oxidative capability of pancreatic tissue, and whether its possible preventive effect involves an antioxidative action of this biocomponent. In this study carried out on rats with acute hemorrhagic pancreatitis induced by 30 min partial pancreatic ischemia followed by 6 h of reperfusion, the GSE or vehicle (vegetable glycerin) was applied intragastrically in gradually increasing amounts (50-500 µl) 30 min before I/R. Pretreatment with GSE decreased the extent of pancreatitis with maximal protective effect of GSE at the dose 250 µl. GSE reduced the pancreatitis-evoked increase in serum lipase and poly-C specific ribonuclease activity, and attenuated the marked fall in pancreatic blood flow and pancreatic DNA synthesis. GSE administered alone increased significantly pancreatic tissue content of lipid peroxidation products, malondialdehyde and 4-hydroxyalkens, and when administered before I/R, GSE reduced the pancreatitis-induced lipid peroxidation. We conclude that GSE exerts protective activity against I/R-induced pancreatitis probably due to the activation of antioxidative mechanisms in the pancreas and the improvement of pancreatic blood flow.
13
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Content available

Expression of transforming growth factor-beta1 and epidermal growth factor in caerulein-induced pancreatitis in rat

59%
Konturek P. C., Dembinski A., Warzecha Z., Ceranowicz P., Konturek S. J., Stachura J., Hahn E. G.
Journal of Physiology and Pharmacology
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1997
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tom 48
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nr 1
14
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Content available

Calcitonin gene-related peptide can attenuate or augment pancreatic damage in caerulein-induced pancreatitis in rats

59%
Warzecha Z., Dembinski A., Ceranowicz P., Konturek P. C., Stachura J., Tomaszewska R., Konturek S. J.
Journal of Physiology and Pharmacology
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1999
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tom 50
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nr 1
15
Artykuł dostępny w postaci pełnego tekstu - kliknij by otworzyć plik
Content available

Protective effect of calcitonin gene-related peptide against caerulein-induced pancreatitis in rats

59%
Warzecha Z., Dembinski A., Ceranowicz P., Konturek P. C., Stachura J., Konturek S. J., Niemiec J.
Journal of Physiology and Pharmacology
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1997
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tom 48
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nr 4
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