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[氧自由基与缺血后器官损伤——病理生理学、临床相关性及治疗]

[Oxygen radicals and postischemic organ damage--pathophysiology, clinical relevance and therapy].

作者信息

Schoenberg M H, Beger H G

机构信息

Abteilung Allgemeine Chirurgie, Universitätsklinik Ulm.

出版信息

Zentralbl Chir. 1995;120(3):174-85.

PMID:7754718
Abstract

Postischemic damages after ischemia and reperfusion are of growing clinical relevance. It was assumed that these damages were due to hypoxia. It has been shown that during reperfusion oxygen radicals are generated in high concentrations adding significantly to the damage. These oxygen radicals are generated by the hypoxanthine-xanthine oxidase system. They do not only damage directly but trigger the accumulation and migration of PMN-leukocytes within the inflicted tissue. PMN-leukocytes induce a non-specific postischemic inflammatory reaction which is responsible for the severe reperfusion damages. Oxygen radicals can be treated successfully by so-called radical scavengers. Thereby, it is essential to initiate the therapy during the so-called "therapeutic window", a time interval in which reperfusion aggravates the ischemic lesions. Only few clinical studies have been performed. The results concerning scavenger treatment after myocardial infarction have been disappointing. In transplantation surgery, however, antioxidative therapy has proven to be beneficial. Well-defined double blind randomized well-stratified clinical studies are now essential in order to assess the possibilities of antioxidative therapy after time-limited ischemia and reperfusion.

摘要

缺血再灌注后的缺血性损伤在临床上的相关性日益增加。过去认为这些损伤是由缺氧所致。现已表明,在再灌注期间会产生高浓度的氧自由基,这显著加重了损伤。这些氧自由基由次黄嘌呤 - 黄嘌呤氧化酶系统产生。它们不仅直接造成损伤,还会引发多形核白细胞(PMN)在受损组织内的聚集和迁移。PMN会引发非特异性的缺血后炎症反应,这是导致严重再灌注损伤的原因。氧自由基可以通过所谓的自由基清除剂成功治疗。因此,必须在所谓的“治疗窗”内开始治疗,“治疗窗”是指再灌注会加重缺血性损伤的一段时间间隔。目前仅进行了少数临床研究。心肌梗死后清除剂治疗的结果并不理想。然而,在移植手术中,抗氧化治疗已被证明是有益的。为了评估限时缺血再灌注后抗氧化治疗的可能性,现在开展明确的双盲随机分层良好的临床研究至关重要。

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