Preferencje help
Widoczny [Schowaj] Abstrakt
Liczba wyników

Znaleziono wyników: 13

Liczba wyników na stronie
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników

Wyniki wyszukiwania

help Sortuj według:

help Ogranicz wyniki do:
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
The aim of this study was to compare the most commonly-used experimental models and to assess the microscopic renal changes in different models of cyclosporine A (CsA) nephrotoxicity. Wistar male rats were divided into five groups, eight animals in each. CsA was given in doses of 15 mg/kg, 25 mg/kg, and 100 mg/kg, respectively. The blood was collected for creatinine, urea, and uric acid levels analysis in the serum and the kidneys were sampled for microscopic examination on the 11th and 29th d of the experiment. CsA induced nephrotoxicity was characterised by increased serum levels of creatinine, urea, and uric acid. Microscopic features of CsA nephrotoxicity in all CsA experimental groups were observed. We would recommend the use of low doses of CsA for approximately 28 d as the most relevant experimental procedure for achieving the features of chronic CsA nephrotoxicity.
The aim of the study was to evaluate blood serum ascorbic acid levels in patients with hepatic cirrhosis, acute and chronic pancreatitis and in the liver, heart, kidneys and lungs of rats intoxicated with CCl₄ and galactosamine. The results revealed statistically significant increases in the blood plasma ascorbic acid levels in patients with acute and chronic pancreatitis and hepatic cirrhosis. In the group of patients with chronic pancreatitis, however, the blood plasma ascorbic acid levels were not different from the controls. In the group of control rats the highest ascorbic acid levels were observed in the liver and the lowest in the heart. In the intoxicated rats with CCl₄ and galactosamine the kidneys’ ascorbic acid contents increased significantly after administration of both toxins in single doses but decreased after 3-days of administration of CCl₄. In the liver, decreased ascorbic acid contents were observed after single doses of CCl4 and galactosamine, but after the 3-day administration its contents were increased. The content of ascorbic acid in the lung increased after each of the toxins used. In the heart, ascorbic acid contents decreased considerably after single and three-day CCl₄ and galactosamine administration as well.
Chronic pancreatitis (CP) is a progressive disease, in which the exocrine function of the gland is gradually lost and fibrosis develops due to repeated episodes of acute pancreatitis. The detection of the renin-angiotensin system (RAS) brings us closer to understanding the pathogenesis of CP. It has been observed that the use of RAS inhibitors reduces hepatic fibrosis. The aim of the study was to examine the effects of RAS inhibitors on fibrotic processes in the course of experimental chronic pancreatitis induced by dibutyltin dichloride (DD). Chronic pancreatitis was induced by administering dibutyltin dichloride to the femoral vein and, simultaneously, captopril, losartan and enalapril which were administered intraperitoneally. The rats were decapitated after 60 days and pancreas tissue was collected for histopathology examination. No pathological changes were observed in the control group. Rats treated by dibutyltin dichloride displayed features of focal inflammatory infiltration, ductal lumen dilatation, fibrosis in the periductal spaces and slight interstitial fibrosis. Animals treated by RAS inhibitor displayed less severe inflammatory changes and fibrosis - particularly those rats treated by enalapril. The findings suggest that enalapril most effectively inhibits inflammatory changes and fibrosis.
Chronic pancreatitis (CP) is a progressive disease, in which the exocrine function of the gland is gradually lost and fibrosis develops due to repeated episodes of acute pancreatitis. The aim of the study was to investigate the effects of RAS inhibitors on the apoptosis of acinar cells and pancreatic stellate cells (PSCs) elimination in experimental CP induced by dibutyltin dichloride (DBTC). CP was induced by administration of DBTC to the femoral vein. Simultaneously captopril, losartan, enalapril and lisinopril were administered intraperitoneally. The rats were decapitated after 60 days and tissue of pancreas was collected. In rats treated by DBTC the features of inflammatory infiltration, ductal lumen dilatation, fibrosis were found. Strong reactivity with capsase2L and clusterin-ß antibodies was observed in areas of fibrosis. In animals treated with RAS inhibitors inflammatory changes and fibrosis were less severe. In groups of rats treated with DBTC and RAS inhibitors immunoreactivity of capsase2L and clusterin-ß was weak. Positive immunostaining against smooth muscle actine and desmin was observed in the elongated cells (PSC-s). This reaction was weak in groups of rat treated with DBTC and RAS inhibitors. Treatment of CP rats with RAS inhibitors alleviate apoptosis of pancreatic acinar cells and induces PSCs elimination.
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.
Pierwsza strona wyników Pięć stron wyników wstecz Poprzednia strona wyników Strona / 1 Następna strona wyników Pięć stron wyników wprzód Ostatnia strona wyników
JavaScript jest wyłączony w Twojej przeglądarce internetowej. Włącz go, a następnie odśwież stronę, aby móc w pełni z niej korzystać.