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

被引:12
|
作者
Subhas, Gokulakkrishna [1 ]
Gupta, Aditya [1 ]
Bakston, Daniel [1 ]
Silberberg, Boris [2 ]
Lobocki, Cathy [3 ]
Andrus, Lee [3 ]
Decker, Melissa [3 ]
Mittal, Vijay K. [1 ]
Jacobs, Michael J. [1 ]
机构
[1] Providence Hosp & Med Ctr, Dept Surg, Southfield, MI USA
[2] Providence Hosp & Med Ctr, Dept Pathol, Southfield, MI USA
[3] Providence Hosp & Med Ctr, Dept Patient Care Res, Southfield, MI USA
来源
AMERICAN JOURNAL OF SURGERY | 2010年 / 199卷 / 03期
关键词
Ischemia-reperfusion injury; Cholestasis; Methylprednisolone; Liver resection; ENDOTHELIAL-CELL INJURY; BILE-DUCT LIGATION; HEPATIC ISCHEMIA/REPERFUSION; EXTENSIVE HEPATECTOMY; PREDNISOLONE; MODEL;
D O I
10.1016/j.amjsurg.2009.09.012
中图分类号
R61 [外科手术学];
学科分类号
摘要
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. (C) 2010 Elsevier Inc. All rights reserved.
引用
收藏
页码:377 / 380
页数:4
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