Is reperfusion injury an important cause of mucosal damage after porcine intestinal ischemia?
Is reperfusion injury an important cause of mucosal damage after porcine intestinal ischemia?
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DOI：
10.1016/s0039-6060(97)90107-0
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发表时间：
1997-05-01
期刊：
影响因子：
3.8
通讯作者：
Argenzio, RA
中科院分区：
文献类型：
--
作者：
Blikslager, AT;Roberts, MC;Argenzio, RA
背景在啮齿动物和猫科动物模型中，由于黄嘌呤氧化酶引发的活性氧代谢物形成和嗜中性粒细胞浸润，再灌注加重了肠缺血性损伤。在幼年猪中进行研究以确定再灌注损伤的相关性，其低水平的黄嘌呤氧化酶与人类相似。通过完全肠系膜动脉闭塞、肠扭转或失血性休克诱导缺血。损伤通过组织学检查和脂质过氧化测定进行评估。此外，还测定了髓过氧化物酶（作为中性粒细胞浸润的标志物）和黄嘌呤氧化酶-黄嘌呤脱氢酶。在肠系膜完全闭塞0.5至3小时或休克或扭转2小时后，明显的缺血性损伤是明显的。在这些模型中，缺血性损伤均未因再灌注而恶化。为了最大限度地产生超氧化物，猪通气100%O-2，但只有有限的再灌注损伤（1.2倍增加组织学分级）。黄嘌呤氧化酶-黄嘌呤脱氢酶In，els可忽略不计（0.4 +/- 0.4 mU/gm）。再灌注损伤在猪肠系膜完全缺血和低流量状态下的肠损伤中可能不起重要作用。这可能是由于低黄嘌呤氧化酶-黄嘌呤脱氢酶水平，这是类似于在人类中发现的。
Background. intestinal ischemic injury is exacerbated by reperfusion in rodent and feline models because of xanthine oxidase-initiated reactive oxygen metabolite formation and neutrophil infiltration. Studies were conducted to determine the relevance of reperfusion injury, in the juvenile pig, whose low levels of xanthine oxidase are similar to those of the human being.Methods. Ischemia was induced by means of complete mesenteric arterial occlusion, volvulus, or hemorrhagic shock. Injury was assessed by means of histologic examination and measurement of lipid peroxidation. In addition, myeloperoxidase, as a marker of neutrophil infiltration, and xanthine oxidase-xanthine dehydrogenase were measured.Results. Significant ischemic injury was evident after 0.5 to 3 hours of complete mesenteric occlusion or 2 hours of shock or volvulus. In none of these models was the ischemic injury worsened by reperfusion. To maximize superoxide production, pigs were ventilated an 100% O-2, but only limited reperfusion injury (1.2-fold increase in histologic grade) was noted. Xanthine oxidase-xanthine dehydrogenase In,els were negligible (0.4 +/- 0.4 mU/gm).Conclusions. Reperfusion injury may not play an important role in intestinal injury under conditions of complete mesenteric ischemia and low-flow states in the pig. This may, result from low xanthine oxidase-xanthine dehydrogenase levels, which are similar to those found in the human being.