Ischemic preconditioning reduces caspase-related intestinal apoptosis

To investigate the preventive effect of ischemic preconditioning (IPC) on ischemia/reperfusion (I/R)-induced apoptosis and injury in the rat intestine. We divided 30 male Wistar rats, weighing 300-350 g, randomly into three groups. The control group rats (n = 10) were subjected to laparotomy only; t...

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Veröffentlicht in:Surgery today (Tokyo, Japan) Japan), 2005-03, Vol.35 (3), p.228-234
Hauptverfasser: Aban, Nedim, Cinel, Leyla, Tamer, Lulufer, Aktas, Atil, Aban, Meral
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Sprache:eng
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Zusammenfassung:To investigate the preventive effect of ischemic preconditioning (IPC) on ischemia/reperfusion (I/R)-induced apoptosis and injury in the rat intestine. We divided 30 male Wistar rats, weighing 300-350 g, randomly into three groups. The control group rats (n = 10) were subjected to laparotomy only; the I/R group (n = 10) rats were subjected to occlusion of the superior mesenteric artery for 45 min, followed by reperfusion for 60 min; and the IPC group (n = 10) rats were subjected to IPC, achieved with two cycles of 5 min ischemia and 5 min reperfusion immediately before the I/R, as in the I/R group. Blood samples were collected by cardiac puncture, to measure nitrate and myeloperoxidase (MPO) levels. Histopathological and immunohistochemical studies were done to evaluate the I/R-induced apoptosis and injury. The blood MPO and nitrate levels were increased in the I/R group, but IPC prevented their increase. There were significantly fewer apoptotic cells in the IPC group than in the I/R group, and this finding was supported by the caspase-3 expression in the ileum. The intestinal histopathology was also protected by IPC against I/R-induced injury. Ischemic preconditioning clearly prevented I/R-induced injury and apoptosis by a mechanism related to the caspase-3-dependent pathway. We also showed that IPC inhibited leukocyte activation, with the suppression of myeloperoxidase levels in I/R and nitric oxide-related oxidoinflammatory pathway upregulation.
ISSN:0941-1291
1436-2813
DOI:10.1007/s00595-004-2918-y