Protective effect of methylprednisolone on warm ischemia-reperfusion injury in a cholestatic rat liver

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...

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Veröffentlicht in:The American journal of surgery 2010-03, Vol.199 (3), p.377-381
Hauptverfasser: Subhas, Gokulakkrishna, M.D., M.R.C.S, Gupta, Aditya, M.D, Bakston, Daniel, M.D, Silberberg, Boris, M.D, Lobocki, Cathy, M.S, Andrus, Lee, L.V.T, Decker, Melissa, L.V.T, Mittal, Vijay K., M.D., F.A.C.S, Jacobs, Michael J., M.D., F.A.C.S
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Sprache:eng
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Zusammenfassung: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.
ISSN:0002-9610
1879-1883
DOI:10.1016/j.amjsurg.2009.09.012