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Am J Surg ; 199(3): 377-80; discussion 380-1, 2010 Mar.
Article in English | MEDLINE | ID: mdl-20226914

ABSTRACT

BACKGROUND: Cholestasis has been identified as a risk factor for oxidative stress, and it potentially enhances after ischemic-reperfusion injury. The aim of this study was to evaluate the role of methylprednisolone on warm ischemia-reperfusion injury in the presence of cholestasis. METHODS: A reversible cholestatic rat model was created. After 7 days, rats received 30 mg/kg of intravenous methylprednisolone 2 hours before ischemia, followed by 30 minutes of ischemia. Rats were euthanized 24 hours after ischemia. Serum aspartate aminotransferase and interleukin-6 were measured, and the liver was harvested for histology and myeloperoxidase estimation. RESULTS: Methylprednisolone had a protective effect, with a statistically significant decrease in aspartate aminotransferase (P=.01) and a trend toward decreased levels of interleukin-6 (P=.07). Histology showed a significant difference in architectural distortion (P=.01), cytoplasmic vacuolation (P=.01), and nodular hepatocellular necrosis (P=.04). CONCLUSIONS: Methylprednisolone attenuated the ischemic-reperfusion injury in the presence of cholestasis and can be considered for clinical use in the presence of cholestasis.


Subject(s)
Cholestasis, Intrahepatic/complications , Glucocorticoids/therapeutic use , Methylprednisolone/therapeutic use , Reperfusion Injury/complications , Reperfusion Injury/prevention & control , Animals , Male , Rats , Rats, Sprague-Dawley , Warm Ischemia
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