烧伤后多器官衰竭及其发病机理中的脂质过氧化损伤

THE ROLE OF LIPID PEROXIDASE INJURY IN THE MECHANISM OF PATHO-GENESIS OF POSTBURN MULTIPLE ORGAN FAILURE

对总体表面积(TBSA)>30％的烧伤患者45例(其中13例并发多器官功能衰竭)进行了前瞻性研究,并连续观察了全血过氧化物歧化酶(SOD)与血浆丙二醛(MDA)含量,以探讨氧自由基的过量释放与脂质过氧化损伤在烧伤后多器官功能衰竭的发病机理中的作用。观察显示,严重烧伤后机体抗氧化能力明显减低,脂质过氧化损伤明显增强。这些改变不仅与烧伤后低容量性休克有关,而且与烧伤及感染的严重程度有关。

Forty-five patients with burn area exceeding 30% TBSA were studied prospectively. Among these 45 patients, 13 developed multiple organ failure (MSOF). Blood superoxide, dismutase (SOD) activity and plasma malondialdehyde (MDA) levels were sequentially determined to assess the role of excessive release of oxygen radicals and lipid peroxidase injury in the mechanism of pathogenesis of postburn MSOF. The results showed that the anti-oxidation capacity of the body was markedly depressed and lipid peroxidase injury markedly increased after a severe burn injury. These changes were not only related to hypovolemic shock after the injury, but also the severity of the burn injury and infection.