Immediate but Not Delayed Postconditioning During Reperfusion Attenuates Acute Lung Injury Induced by Intestinal Ischemia/Reperfusion in Rats: Comparison with Ischemic Preconditioning
Immediate but Not Delayed Postconditioning During Reperfusion Attenuates Acute Lung Injury Induced by Intestinal Ischemia/Reperfusion in Rats: Comparison with Ischemic Preconditioning
复制标题
DOI：
10.1016/j.jss.2008.11.843
复制
发表时间：
2009-11-01
影响因子：
2.2
通讯作者：
Li, Yi
中科院分区：
文献类型：
--
作者：
Liu, Ke-Xuan;Li, Yun-Sheng;Li, Yi
背景先前的研究已经表明，在再灌注开始时施加的短暂的重复性上级肠系膜动脉（SMA）闭塞和再灌注，即缺血后处理（IPo），减轻了肠缺血/再灌注（II/R）后的肠损伤。本研究验证了IPo会减轻II/R诱导的急性肺损伤的假设，这与缺血预处理（IPC）相当，并且在再灌注开始时应用的短暂后处理对IPo的肺保护至关重要。采用夹闭SMA 60 min再灌注60 min的方法造成大鼠II/R损伤。将大鼠随机分为5组（n = 8）：假手术组（Sham）：进行假手术准备，包括不阻断SMA，损伤组：SMA阻断前或阻断后均不进行干预，缺血预处理组（IPC）：SMA阻断10 min，再灌注10 min，再延长阻断时间;缺血后处理（IPo）：再灌注后立即进行30秒再灌注-30秒再闭塞的三个循环（3分钟总干预）;延迟后处理：完全释放钳夹以完全再灌注3分钟（IPo算法的持续时间），之后进行30秒闭塞和再灌注的三个循环。肺组织学检查显示，损伤组大鼠肺组织严重损伤，表现为肺湿/干重比和肺通透性指数增加，血浆TNF α和IL-6水平升高，肺组织丙二醛（MDA）含量升高，髓过氧化物酶（MPO）活性升高，超氧化物歧化酶（SOD）活性降低。IPo能明显减轻肺损伤，改善上述指标，与IPC相当。IPo在再灌注开始时减少由II/R诱导的急性肺损伤，这可能部分地通过抑制氧化剂产生、中性粒细胞过滤和促炎介质释放来介导。在大鼠模型中，再灌注早期是IPo肺保护的关键。IPo可改善II/R相关临床状况的结局。(C)2009 Elsevier Inc. All rights reserved.
Background. A previous study has shown that brief period of repetitive superior mesenteric artery (SMA) occlusion and reperfusion applied at the onset of reperfusion, ischemic postconditioning (IPo), attenuates intestinal injury after intestinal ischemia/reperfusion (II/R). This study tested the hypothesis that IPo would attenuate II/R-induced acute lung injury, which is comparable to ischemic preconditioning (IPC) and the brief period of postconditioning applied at the onset of reperfusion is critical to pulmonary protection by IPo.Methods. Rat II/R injury was produced by clamping SMA for 60 min followed by 60 min of reperfusion. The rats were randomly allocated into one of five groups based upon the intervention (n = 8): sham operation (Sham): sham surgical preparation including isolation of the SMA without occlusion was performed; Injury: there was no intervention either before or after SMA occlusion; ischemia preconditioning (IPC): the SMA was occluded for 10 min followed by 10 min of reperfusion before prolonged occlusion; ischemia postconditioning (IPo): three cycles of 30 sec reperfusion-30 sec reocclusion were imposed immediately upon reperfusion (3 min total intervention); delayed postconditioning: clamping was completely released for full reperfusion for 3 min (the duration of the IPo algorithm), after which three cycles of 30 sec occlusion and reperfusion were applied.Results. Histologic results showed severe damage in rat lungs in the injury group evidenced by increased lung wet/dry weight ratio and pulmonary permeability index, which was accompanied by increases in the levels of plasma TNF alpha and IL-6, the pulmonary malondialdehyde (MDA), and the pulmonary myeloperoxidase (MPO) activity and a decrease in superoxide dismutase (SOD) activity. IPo, not delayed IPo, could significantly attenuate lung injury and improve the above variables, which was comparable to IPC.Conclusions. IPo at onset of reperfusion reduces acute lung injury induced by II/R, which may be mediated, in part, by inhibiting oxidant generation, neutrophils filtration, and proinflammatory mediators releases. The early period of reperfusion in the rat model is critical to pulmonary protection by IPo. IPo may improve outcome in clinical conditions associated with II/R. (C) 2009 Elsevier Inc. All rights reserved.