Ischemic preconditioning protects against gut dysfunction and mucosal injury after ischemia/reperfusion injury
Ischemic preconditioning protects against gut dysfunction and mucosal injury after ischemia/reperfusion injury
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DOI：
10.1097/01.shk.0000155195.17687.00
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发表时间：
2005-03-01
期刊：
影响因子：
3.1
通讯作者：
Kone, BC
中科院分区：
文献类型：
--
作者：
Moore-Olufemi, SD;Kozar, RA;Kone, BC
肠系膜缺血再灌注(IR)损伤胃肠道上皮细胞，损害肠道功能。缺血预适应(IPC)已被证明具有保护器官免受IR损伤的作用。我们假设IPC保护肠道免受IR损伤。将大鼠随机分为假手术组、假手术组、假手术组和晚期假手术组。SMA阻断30min，再灌流6h)。在6h时，测定中转点，并表示为平均几何中心。取回肠行黏膜损伤和髓过氧化物酶活性测定。用湿/干重量比测定组织水来评估肠道水肿。与假的早期IPC+IR组相比，早期PC+IR组显著改善转运(3.9+/-0.2)，降低MPO水平(3+/-2)，减轻粘膜损伤(1.2+/-0.3)(转运，2.9+/-0.2；MPO水平，9+/-1；粘膜损伤，3.0+/-0.6)。晚期IPC+IR较假手术晚期IPC+IR(TRANS4.4+/-0.2；MPO水平8+/-1)转运(6.0+/-0.4)显著增加，MPO(1+/-1)降低(1+/-1)，但在黏膜保护方面与假手术晚期IPC+IR(1+/-1)无差异。我们的结果表明，早期和晚期的IPC改善了肠功能障碍，减少了炎症，并对IR后的肠道提供了粘膜保护。我们的结果表明，IPC可以改善IR引起的肠道功能障碍。IPC的这两个阶段在外科病人护理的临床环境中都可能是有用的。
Mesenteric ischemia/reperfusion (IR) damages the gastrointestinal epithelia and impairs gut function. Ischemic preconditioning (IPC) has been shown to protect organs against IR injury. We hypothesized that IPC protects the gut from IR injury. Rats were randomized to a sham group, a sham early IPC + IR group (sham IPC + SMA occlusion for 30 min and 6 h of reperfusion), an early IPC + IR group (IPC, three cycles of SMA occlusion for 4 min and reperfusion for 10 min) followed immediately by SMA occlusion for 30 min and 6 h of reperfusion), a sham 24-h group, a sham late IPC + IR group (sham IPC followed by additional reperfusion for 24 h + SMA occlusion for 30 min and 6 h of reperfusion), and a late IPC + IR group ([PC protocol followed by additional reperfusion for 24 h, and then SMA occlusion for 30 min followed by 6 h of reperfusion). At 6 h, transit was determined and expressed as the mean geometric center. Ileum was harvested for assessment of mucosal injury and myeloperoxidase (MPO) activity. Tissue water was determined using the wet-to-dry weight ratio to assess gut edema. Early]PC + IR significantly improved transit (3.9 +/- 0.2), decreased MPO levels (3 +/- 2), and lessened mucosal injury (1.2 +/- 0.3) compared with animals subjected to sham early IPC + IR (transit, 2.9 +/- 0.2; MPO levels, 9 +/- 1; mucosal injury, 3.0 +/- 0.6). Late IPC + IR also improved transit (6.0 +/- 0.4) and decreased MPO levels (1 +/- 1) compared with sham late IPC + IR (transit, 4.4 +/- 0.2; MPO levels, 8 +/- 1), however, there was no difference in the mucosal protection between late IPC + IR (1 +/- 0.3) and sham late IPC + IR (1 +/- 1). Our results suggest that early and late IPC improves intestinal dysfunction, decreases inflammation, and provides mucosal protection in the intestine after IR. Our results show that IR-induced gut dysfunction can be improved by IPC. Both phases of IPC can potentially be useful in the clinical setting of surgical patient care.