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The protective effect of ischemic preconditioning on small intestinal ischemia-reperfusion injury

缺血预处理对小肠缺血再灌注损伤的保护作用

基本信息

批准号：
13671315
负责人：
HAMADA Nobuo
金额：
$ 2.11万
依托单位：
Kagoshima University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2001
资助国家：
日本
起止时间：
2001 至 2002
项目状态：
已结题

项目摘要

While ischemic preconditioning (IP) has been shown to have protective effect for ischemia-reperfusion injury (IRI) in several organ systems, little is known about the effect on intestinal IRI. In this study, we investigated the immediate protective effect of IP on intestinal IRI.The entire canine small intestine was isolated on a vascular pedicle that consisted of the proximal superior mesenteric artery and vein. Complete intestinal warm ischemia was induced by clamping these vessels. The dogs were randomized into four groups (each n=5) : Group I -control group, animals subjected to 120 min of intestinal ischemia, followed by 240 min of reperfusion. Group II -ischemic preconditioning group (IP) : Before the ischemia reperfusion period (as in group I), animals were subjected to previous ischemic preconditioning with 15 min of ischemia and 15 min of reperfusion. Group III -nicorandil (Nic) treated group, same as group I, but nicorandil, a selective K_<ATP> channel opener, was given to animals with bolus injection of 100 μg/kg/min during the reperfusion. Group IV -glibenclamide (Gli) treated group, same as group II, but 0.3 mg/kg of glibenclamide, selective K_<ATP> channel blocker, was given intravenously 15 min before IPC.Compared to the control, the preconditioned group reduced CPK and lactate levels in the portal vein, maintained the intestinal mucosal pH (pHi) and attenuated the histological tissue damage after reperfusion. Nic treatment showed better outcome of pHi, and Gli administration attenuated the ischemic preconditioning effect.These results suggest that IP can protect the intestine from the prolonged ischemia and reperfusion injury and that the K_<ATP> channel plays an important role in this protection mechanism.

虽然缺血预处理（IP）已被证明对多个器官系统的缺血再灌注损伤（IRI）具有保护作用，但对肠IRI的影响知之甚少。在这项研究中，我们研究了IP对肠道IRI的即时保护作用。整个犬小肠分离的血管蒂，包括近端上级肠系膜动脉和静脉。通过夹闭这些血管诱导完全肠热缺血。将狗随机分为四组（每组n=5）：I组-对照组，动物经受120分钟的肠缺血，随后再灌注240分钟。II组-缺血预处理组（IP组）：在缺血再灌注期前（同I组），动物接受预先缺血预处理，即缺血15 min，再灌注15 min。尼可地尔（Nic）治疗组，<ATP>在再灌注期间给予选择性钾通道开放剂尼可地尔100 μg/kg/min。IV组-格列本脲（Gli）治疗组，与II组相同，但在<ATP>IPC前15 min静脉注射选择性钾通道阻滞剂格列本脲0.3mg/kg。与对照组相比，预处理组降低门静脉CPK和乳酸水平，维持肠粘膜pH（pHi），减轻再灌注后组织学损伤。结果表明，IP对肠缺血再灌注损伤具有保护作用，K<ATP>通道在此保护机制中起重要作用。