Trigger for intercellular adhesion molecule-1 expression in rat lungs transplanted from non-heart-beating donors.
Trigger for intercellular adhesion molecule-1 expression in rat lungs transplanted from non-heart-beating donors.
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在无心跳供体移植的大鼠肺中触发细胞间粘附分子 1 的表达。
DOI：
10.1016/j.athoracsur.2003.08.023
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发表时间：
2004
期刊：
影响因子：
--
通讯作者：
Davis,ClarenceE
中科院分区：
文献类型：
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作者：
Egan,ThomasM;Thomas,Yalaunda;Gibson,Debra;Funkhouser,William;Ciriaco,Paola;Kiser,Andy;Sadoff,John;Bleiweis,Mark;Davis,ClarenceE
研究背景无心跳供体的肺移植会引起缺血再灌注损伤。我们试图确定缺血再灌注损伤引起的细胞间粘附分子-1（ICAM-1）表达的触发因素。方法36只Sprague-Dawley大鼠接受左肺移植（6组，每组6只）。肺移植后立即逮捕，或无心跳供体后2小时的氧气通气或无通气。受体再灌注4或6小时，然后用小鼠抗大鼠ICAM-1单克隆抗体染色，用抗生物素蛋白-生物素过氧化物酶显影为生物素化的抗小鼠免疫球蛋白G抗体。细胞间粘附分子-1的表达由两名蒙面观察员分级为0 =无，1 =弱，或2 =肺泡，小动脉和小静脉强。移植的受体左肺作为阴性对照，腹腔内注射内毒素后6小时产生阳性对照。各组间细胞间粘附分子-1的表达均高于基线水平，采用Fisher精确检验，结果显示：大鼠肺泡内ICAM-1呈组成型表达，对照组中24例呈弱阳性表达，4例呈强阳性表达。再灌注4小时后评估的移植肺中细胞间粘附分子-1表达没有增加，即使是从无心跳供体中取出的肺。但是，当非心脏跳动供体肺进行评估6小时后再灌注，ICAM-1的表达显着更明显的肺泡和小动脉区，与对照组和肺移植后立即arrest.CONCLUSIONSLungs移植后立即停循环不维持足够的缺血再灌注损伤上调ICAM-1。再灌注的开始是ICAM-1表达的信号，而不是缺血的开始或缺血和再灌注的总持续时间。再灌注策略可使ICAM-1表达最小化。
BACKGROUNDLung transplantation from non–heart-beating donors causes ischemia-reperfusion injury. We sought to determine the trigger for expression of intercellular adhesion molecule-1 (ICAM-1) caused by ischemia-reperfusion injury.METHODSThirty-six Sprague-Dawley rats underwent left lung transplant (six groups of 6). Lungs were transplanted immediately after arrest, or from non–heart-beating donors after 2 hours of oxygen-ventilation or no ventilation. Recipients were reperfused for 4 or 6 hours, then lungs were stained with a mouse anti-rat ICAM-1 monoclonal antibody, developed with avidin-biotin peroxidase to a biotinylated anti-mouse immunoglobin G antibody. Intercellular adhesion molecule-1 expression was graded by two masked observers as 0 = absent, 1 = weak, or 2 = strong in alveoli, arterioles, and venules. Explanted recipient left lungs served as negative controls, and positive controls were generated 6 hours after intraperitoneal injection of endotoxin. Intercellular adhesion molecule-1 expression above baseline among groups was compared by Fisher's exact test.RESULTSConstitutive expression of ICAM-1 was present in rat lung alveoli, with 24 of 35 controls staining weakly and 4 of 35 strongly positive in alveolar areas. Intercellular adhesion molecule-1 expression was not increased in transplanted lungs evaluated after 4 hours of reperfusion, even lungs retrieved from non–heart-beating donors. But when non–heart-beating donor lungs were assessed 6 hours after onset of reperfusion, ICAM-1 expression was significantly more apparent in alveolar and arteriolar areas, compared with controls and lungs transplanted immediately after arrest.CONCLUSIONSLungs transplanted immediately after circulatory arrest do not sustain sufficient ischemia-reperfusion injury to upregulate ICAM-1. Onset of reperfusion is the signal for ICAM-1 expression, not the onset of ischemia or the total duration of ischemic and reperfusion time together. Strategies at reperfusion may minimize ICAM-1 expression.