Cicalese L, Caraceni P, Nalesnik M A, Borle A B, Schraut W H
Pittsburgh Transplantation Institute, Pennsylvania 15213, USA.
Transplantation. 1996 Jul 27;62(2):161-6. doi: 10.1097/00007890-199607270-00003.
Mucosal injury is an immediate event following revascularization of small intestinal grafts in the context of transplantation (SBTx). The generation of oxygen free radicals (OFR) and tissue infiltration by activated neutrophils are consequences of ischemia and reperfusion and known causative factors of tissue injury; to delineate their role in the reperfusion injury occurring after cold preservation of the intestine and subsequent transplantation was the aim of this study. Prior to orthotopic SBTx in Sprague-Dawley rats, grafts were stored in cold (4 degrees C) Ringer's lactate solution for 1 (n=6), 2 (n=7), and 4 hr (n=7). Small bowel biopsy specimens were obtained before harvesting, at the end of the (cold) ischemic period and immediately before unclamping (i.e., before revascularization) and 30, 60, 120 min, and 24 hr after transplantation to evaluate tissue injury by histology, OFR production, (measured by luminol-enhanced chemiluminescence [LCL]), and the degree of neutrophil infiltration by myeloperoxidase staining. Reperfusion of the graft significantly worsened the histologically graded mucosal injury compared with that seen before unclamping. However, 24 hr after engraftment, mucosal morphology was restored almost completely. OFR production increased significantly during the early phases of reperfusion (30, 60, and 120 min) and returned to control values after 24 hr. Reperfusion of the graft was associated with a marked increase in the number of mucosal neutrophils. The present study indicates that OFR production and neutrophilic infiltration commence and progressively increase with graft reperfusion. These changes parallel the mucosal injury. Ischemic intervals of 4 hr were not associated with a statistically significant greater ischemic-injury patterns compared with 1- and 2-hr intervals. The profound changes associated with reperfusion probably overshadow the minor, yet likely, progressive injury patterns associated with longer ischemia times.
在小肠移植（SBTx）过程中，黏膜损伤是小肠移植物血管重建后的即刻事件。氧自由基（OFR）的产生以及活化中性粒细胞的组织浸润是缺血和再灌注的后果，也是已知的组织损伤致病因素；本研究的目的是明确它们在肠道冷藏及后续移植后发生的再灌注损伤中的作用。在将Sprague-Dawley大鼠进行原位SBTx之前，将移植物置于冷（4℃）乳酸林格液中保存1小时（n = 6）、2小时（n = 7）和4小时（n = 7）。在收获前、（冷）缺血期末、松开血管夹前（即血管重建前）以及移植后30、60、120分钟和24小时获取小肠活检标本，通过组织学、OFR产生（通过鲁米诺增强化学发光法[LCL]测量）以及髓过氧化物酶染色评估中性粒细胞浸润程度来评估组织损伤。与松开血管夹前相比，移植物再灌注使组织学分级的黏膜损伤明显加重。然而，植入后24小时，黏膜形态几乎完全恢复。再灌注早期（30、60和120分钟）OFR产生显著增加，24小时后恢复至对照值。移植物再灌注与黏膜中性粒细胞数量显著增加有关。本研究表明，OFR产生和中性粒细胞浸润随着移植物再灌注开始并逐渐增加。这些变化与黏膜损伤平行。与1小时和2小时的缺血间隔相比，4小时的缺血间隔在统计学上与更大的缺血损伤模式无关。与再灌注相关的深刻变化可能掩盖了与较长缺血时间相关的轻微但可能的渐进性损伤模式。
