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Query: UMLS:C0030305 (
pancreatitis
)
16,014
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
The effect of methylprednisolone on hemodynamics and oxygen transport was investigated in acute hemorrhagic
pancreatitis
in 13 dogs randomly allocated to a fluid treatment group, a methylprednisolone prophylaxis (MPP) group and a methylprednisolone therapy (MP) group.
Methylprednisolone
(30 mg/kg) was given as a bolus dose, starting 30 min before induction of
pancreatitis
in the MPP group and 30 min after induction in the MP group. Acute hemorrhagic pancreatitis was induced with a mixture of trypsin and sodium taurocholate, and hemodynamics and blood gases were monitored for 4.5 hours. MPP improved cardiac output significantly and prevented the initial increase in the arteriovenous oxygen content difference. In the MP group there were no significant differences from the control group in hemodynamics or oxygen transport. Prophylactically administered methylprednisolone thus partially attenuated the hemodynamic changes caused by acute hemorrhagic
pancreatitis
. It seemed especially to improve cardiac performance, assessed from changes in cardiac output.
...
PMID:Methylprednisolone in acute canine hemorrhagic pancreatitis. 335 81
Glucocorticoids are potent anti-inflammatory drugs. The molecular mechanisms underlying these effects have not yet been fully revealed. The aim of the present study was to establish whether methylprednisolone pretreatment is beneficial and if it can block the pancreatic DNA binding of the transcription factor nuclear factor-kappaB (NF-kappaB) and proinflammatory cytokine synthesis during cholecystokinin-octapeptide (CCK)-induced acute pancreatitis in rats. Additionally, we set out to investigate the potential effects of methylprednisolone and CCK on pancreatic heat shock protein (HSP) synthesis. The dose-response (5-40 mg/kg) and time-course (6-72 h) curves of methylprednisolone on pancreatic HSP60 and HSP72 synthesis were evaluated following methylprednisolone treatment. We demonstrated that methylprednisolone specifically and dose-dependently induced HSP72 in the pancreas of rats, while it did not have a significant effect on HSP60 expression. The
pancreatitis
was induced near the peak level of HSP72 synthesis (2 x 30 mg/kg body weight [b.w.] methylprednisolone i.m. at an interval of 12 h, followed by a 12-h recovery period after the second injection of methylprednisolone) by administering 2 x 100 microg/kg CCK subcutaneously at an interval of 1 h. The injections of CCK in the vehicle-pretreated group significantly elevated the levels of pancreatic HSP60 and HSP72 2-4 h after the second CCK injection.
Methylprednisolone
pretreatment ameliorated many of the examined laboratory (the pancreatic weight/body weight [p.w./b.w.] ratio, the serum amylase activity, the plasma trypsinogen activation peptide concentration, the pancreatic levels of tumor necrosis factor-alpha and interleukin-6, the degree of lipid peroxidation, protein oxidation, nonprotein sulfhydryl group content and the pancreatic myeloperoxidase activity) and morphological parameters of the disease.
Methylprednisolone
pretreatment did not influence pancreatic NF-kappaB DNA binding, but decreased proinflammatory cytokine synthesis in this acute pancreatitis model. The findings suggest that the anti-inflammatory effect of large doses of methylprednisolone in secretagogue-induced
pancreatitis
occurs downstream of NF-kappaB DNA binding, and that increased pancreatic HSP72 synthesis may play a role in the protective effect of the drug.
...
PMID:The anti-inflammatory effect of methylprednisolone occurs down-stream of nuclear factor-kappaB DNA binding in acute pancreatitis. 1262 May 16