Protective effects of ischemic preconditioning on the intestinal mucosal microcirculation following ischemia-reperfusion of the intestine

被引:27
作者
Mallick, IH
Yang, WY
Winslet, MC
Seifalian, AM
机构
[1] UCL, Acad Div Surg & Intervent Sci, GI & Hepatobiliary Res Lab, London NW3 2PF, England
[2] Royal Free Hampstead NHS Trust Hosp, London, England
关键词
heme oxygenase; intravital microscopy; reperfusion injury; zinc protoporphyrin; small bowel;
D O I
10.1080/10739680500301631
中图分类号
R5 [内科学];
学科分类号
1002 ; 100201 ;
摘要
Objective: The small bowel villi are extremely sensitive to ischemia-reperfusion (IR) injury and a range of microcirculatory disturbances contribute to structural and functional changes. The aim of this study was to determine the protective effects of ischemic preconditioning (IPC) of the intestine on the mucosal villous microcirculation during IR injury of the intestine and whether heme oxygenase (HO) is involved in the protection. Methods: Rats were allocated into 4 groups: (1) sham, (2) IR consisting of 30 min of ischemia followed by 2 h of reperfusion, (3) IPC, as in IR group, but preceded by 10 min of ischemia and 10 min of reperfusion, and (4) with administration of zinc protoporphyrin, an HO inhibitor before IPC and IR. The mucosa of an exteriorized segment of ileum was visualized. Mucosal perfusion index (MPI), red blood cell (RBC) velocity and leukocyte-endothelial interactions during reperfusion were assessed continuously using in vivo fluorescence microscopy. HO activity in the ileum was assessed at the end of the reperfusion period. Results: IPC improved the MPI by 26% and the RBC velocity by 29% on comparison to IR. IR led to a 52% increase in leukocyte-endothelial interactions on comparison to IPC. The administration of zinc protoporphyrin reversed the beneficial effects of IPC. There was a two fold increase of HO activity in IPC compared to IR, whereas zinc protoporphyrin significantly reduced the HO activity. Conclusions: IPC conferred a protective effect on the villous microcirculation possibly via HO and might prove to be an effective strategy for the amelioration of IR injury.
引用
收藏
页码:615 / 625
页数:11
相关论文
共 40 条
[1]  
Aksöyek S, 2002, SHOCK, V18, P476
[2]  
[Anonymous], FREE RADICALS BIOL M
[3]   Heme oxygenase-1 induction by hemin protects against gut ischemia/reperfusion injury [J].
Attuwaybi, BO ;
Kozar, RA ;
Moore-Olufemi, SD ;
Sato, N ;
Hassoun, HT ;
Weisbrodt, NW ;
Moore, FA .
JOURNAL OF SURGICAL RESEARCH, 2004, 118 (01) :53-57
[4]  
BALLA G, 1992, J BIOL CHEM, V267, P18148
[5]   Heme oxygenase-1: Redox regulation and role in the hepatic response to oxidative stress [J].
Bauer, M ;
Bauer, I .
ANTIOXIDANTS & REDOX SIGNALING, 2002, 4 (05) :749-758
[6]  
BRUNE B, 1987, MOL PHARMACOL, V32, P497
[7]  
Chien S, 1982, Adv Shock Res, V8, P71
[8]  
CHIU CJ, 1970, ARCH SURG-CHICAGO, V101, P478
[9]   Ischemic preconditioning reduces intestinal epithelial apoptosis in rats [J].
Cinel, I ;
Avlan, D ;
Cinel, L ;
Polat, G ;
Atici, S ;
Mavioglu, I ;
Serinol, H ;
Aksoyek, S ;
Oral, U .
SHOCK, 2003, 19 (06) :588-592
[10]  
CLASTER S, 1984, BLOOD, V64, P1079