Ischemic preconditioning and methylprednisolone both equally reduce hepatic ischemia/reperfusion injury

被引:51
|
作者
Glanemann, M [1 ]
Strenziok, R [1 ]
Kuntze, R [1 ]
Münchow, S [1 ]
Dikopoulos, N [1 ]
Lippek, F [1 ]
Langrehr, JM [1 ]
Dietel, M [1 ]
Neuhaus, P [1 ]
Nussler, AK [1 ]
机构
[1] Humboldt Univ, Charite, Dept Gen Visceral & Transplantat Surg, D-13353 Berlin, Germany
关键词
D O I
10.1016/j.surg.2003.08.011
中图分类号
R61 [外科手术学];
学科分类号
摘要
Background. Ischemic preconditioning (I/P) and methylprednisolone (W) have been suggested to Protect against ischemia-reperfusion (IR) injury, which results in an increased tolerance against organ hypoxia. Methods. Before 45 minutes of hepatic ischemia, male Wistar rats were pretreated with either I/P (5130 minutes) or MP (30 mg/kg BW). The degree of IR injury and the postischemic inflammatory (leukocyte infiltration, myeloperoxidase, intercellular adhesion molecule-1) and apoptotic (TUNEL, caspase 3, cytochrome C) activity was measured in both groups and compared with non-pretreated (ischemic) animals. Results. Histology and enzyme release revealed that I/P and MP treatment provided significant protection as compared with ischemic controls. TUNEL-positive cells, as well, as caspase 3 and cytochrome C expression, were clearly reduced in hepatic tissue of MP-treated animals and partially reduced in I/P-treated animals when compared with ischemic animals. The inflammatory response was considerably reduced in MP- and I/P-treated animals, especially in the early period after ischemia. NF-kappaB/Rel-binding activity was increased after I/P and decreased in MP-treated animals, whereas ischemic controls showed a constant binding activity. Conclusions. MP (probably by downregulation of NF-kappaB-binding activity) and I/P attenuated the postischemic apoptotic and inflammatory response. Both treatments equally reduced M-related hepatocellular damage, and, thus, may also be applied equally in surgery involving warm organ hypoxia.
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页码:203 / 214
页数:12
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