title: Immediate postconditioning during reperfusion attenuates intestinal injury.
abstract: OBJECTIVE
  To test the hypothesis that immediate but not delayed ischemic postconditioning (IPo) during reperfusion attenuates intestinal injury, and that ischemic preconditioning (IPC) and IPo may confer synergy in intestinal protection.
  
  
  METHODS
  Prospective laboratory animal study with concurrent control.
  
  
  METHODS
  Adult Sprague-Dawley rats.
  
  
  METHODS
  Intestinal ischemia/reperfusion (II/R) injury in rats was produced by clamping superior mesenteric artery for 60 min followed by 60 min reperfusion; IPC was elicited by 10 min ischemia and 10 min reperfusion before index ischemia; IPo was performed by three cycles of 30 s reperfusion and 30 s ischemia initiated either immediately at the onset of reperfusion (IPo) or after reperfusion for 3 min (delayed-IPo). Combination of IPC and IPo was performed by combining both protocols.
  
  
  RESULTS
  Intestinal ischemia/reperfusion resulted in significant intestinal injury evidenced as significant increase in Chiu's scores and wet-to-dry intestine weight ratio accompanied with increases in plasma levels of tumor necrosis factor-alpha and interleukin-6, as well as increases in the intestinal tissue lipid peroxidation product malonediadehyde and myeloperoxidase activity as compared to control animals (all P < 0.05). All these changes were significantly attenuated either by IPC or IPo or their combination (P < 0.05), and not by delayed-IPo (P > 0.05). IPC and IPo showed synergistic protection compared with either protocol alone.
  
  
  CONCLUSIONS
  Ischemic postconditioning reduces intestinal injury, in part, by inhibiting oxidative injury, neutrophils filtration and proinflammatory response. The early period of reperfusion is critical to intestinal protection by IPo, and intestinal protection with IPo can be enhanced by IPC.
authors.affiliation: Department of Anesthesiology, The First Affiliated Hospital, Sun Yat-sen University, No. 58, Zhongshan 2th Road, 510080 Guangzhou, China. liukexuan807@yahoo.com.cn
authors.forename: Ke-Xuan
authors.initials: KX
authors.lastname: Liu
authors.forename: Yun-Sheng
authors.initials: YS
authors.lastname: Li
authors.forename: Wen-Qi
authors.initials: WQ
authors.lastname: Huang
authors.forename: Shu-Qing
authors.initials: SQ
authors.lastname: Chen
authors.forename: Zhong-Xin
authors.initials: ZX
authors.lastname: Wang
authors.forename: Jia-Xin
authors.initials: JX
authors.lastname: Liu
authors.forename: Zhengyuan
authors.initials: Z
authors.lastname: Xia
mesh_terms: D000818:Animals; D003213:Conditioning, Psychological; D015850:Interleukin-6 / Q000097:blood; D007413:Intestinal Mucosa / Q000378:metabolism; D007422:Intestines / Q000098:blood supply* / Q000293:injuries*; D007511:Ischemia / Q000503:physiopathology; D015227:Lipid Peroxidation; D008297:Male; D008315:Malondialdehyde / Q000378:metabolism; D009504:Neutrophils / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D011446:Prospective Studies; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000097:blood* / Q000378:metabolism; D014409:Tumor Necrosis Factor-alpha / Q000097:blood
chemical_list: D015850:Interleukin-6; D014409:Tumor Necrosis Factor-alpha; D008315:Malondialdehyde