Rauen U, Viebahn R, Lauchart W, de Groot H
Institut für Physiologische Chemie, Universitätsklinikum Essen, Germany.
Hepatogastroenterology. 1994 Aug;41(4):333-6.
Reperfusion of a previously ischemic tissue may lead to an aggravation of injury. The liver has been shown to be susceptible to this reperfusion injury in several experimental systems. Reactive oxygen species appear to play an important role in the development of such injury, as has been demonstrated by direct measurements of their release, and by the protective effects of antioxidants. Upon reperfusion, reactive oxygen species may be released by hepatocytes, Kupffer cells and neutrophils. The relative contribution of the various liver cell types to the release of reactive oxygen species depends on several factors, including the duration and condition of ischemia and the time elapsed after reperfusion. There is only limited evidence for the occurrence of reperfusion injury in humans following liver surgery. The role of reactive oxygen species in this injury in humans remains to be shown.
先前缺血组织的再灌注可能会导致损伤加重。在多个实验系统中，肝脏已被证明易受这种再灌注损伤的影响。活性氧似乎在这种损伤的发展中起重要作用，这已通过直接测量其释放以及抗氧化剂的保护作用得到证实。再灌注时，活性氧可能由肝细胞、库普弗细胞和中性粒细胞释放。各种肝细胞类型对活性氧释放的相对贡献取决于几个因素，包括缺血的持续时间和状况以及再灌注后经过的时间。关于肝脏手术后人类发生再灌注损伤的证据有限。活性氧在人类这种损伤中的作用仍有待证实。
