Schoenberg M H, Beger H G
Dept. of General Surgery, University of Ulm, F.R.G.
Chem Biol Interact. 1990;76(2):141-61. doi: 10.1016/0009-2797(90)90085-2.
Intestinal ischemia, however, caused, is still a serious and growing clinical problem with an unacceptable mortality rate of over 60%. This high mortality rate is mainly due to the fact that the patients are not admitted to the hospital or not treated early enough. Even if the patients are operated on within 24 h, their mortality rate is still over 50%, and those surviving the initial treatment suffer from postischemic complications. These damages have been accounted until now to tissue ischemia. It has been proven experimentally that also reperfusion or revascularization after time-limited ischemia add to the tissue damages observed, due to the formation of O2-radicals. Thereby the prerequisites for the production of these radicals (the conversion of xanthine dehydrogenase to xanthine oxidase and the increase of hypoxanthine concentrations in the tissue and plasma) are generated during tissue ischemia. These radicals damage directly or initiate several vicious circles leading to mucosal lesions, impaired intestinal function and an enhanced absorption of bacteria and endotoxin. Various substances (SOD, catalase, DMSO, allopurinol, deferoxamine etc.) detoxify oxygen radicals or inhibit the pathomechanisms leading to the enhanced radical generation. Hopefully, the combination of early revascularization with these already available scavengers will improve the high mortality and morbidity of patients suffering from intestinal ischemia.
然而，肠道缺血仍然是一个严重且日益突出的临床问题，其死亡率超过60%，令人难以接受。这种高死亡率主要是因为患者未及时入院或未得到足够早的治疗。即使患者在24小时内接受手术，其死亡率仍超过50%，且那些在初始治疗中存活下来的患者会出现缺血后并发症。到目前为止，这些损伤一直被认为是由组织缺血导致的。实验已经证明，在限时缺血后的再灌注或血管重建也会由于氧自由基的形成而加重所观察到的组织损伤。由此，这些自由基产生的先决条件（黄嘌呤脱氢酶转化为黄嘌呤氧化酶以及组织和血浆中次黄嘌呤浓度的增加）在组织缺血期间产生。这些自由基直接造成损害或引发几个恶性循环，导致黏膜损伤、肠道功能受损以及细菌和内毒素吸收增加。各种物质（超氧化物歧化酶、过氧化氢酶、二甲基亚砜、别嘌呤醇、去铁胺等）可清除氧自由基或抑制导致自由基生成增加的发病机制。有望将早期血管重建与这些现有的清除剂相结合，改善肠道缺血患者的高死亡率和高发病率。
