术中自体机械输血时血液中脂质过氧化(LPO)的启动——脂质过氧化产物的肝毒性是否具有临床意义?

Anaesthesiologie und Reanimation Pub Date : 2000-01-01
M Kretzschmar, M Münster, W Schirrmeister
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引用次数: 0

摘要

在广泛的外科手术过程中,使用细胞保存器的机器自身输血是一种成熟的保存同种血液的方法。血液的加工可诱导脂质过氧化(LPO)的启动,并释放肝毒性产物。研究组由42例接受初次(n = 20)或翻修(n = 22)髋关节置换术的患者组成。患者平均接受1260毫升的自体血液和2.2单位的同源填充细胞。测定患者血浆、自体填充细胞和细胞保存剂处理后的血液上清液中作为LPO代谢物的硫代巴比妥酸反应性物质(TBARS)的浓度。此外,还测定了铁代谢参数、血红蛋白水平、红细胞压积以及所谓的肝酶——天冬氨酸转氨酶、丙氨酸转氨酶、γ -谷氨酰转肽酶和胆碱酯酶的活性。在机器自体输血过程中可检测到LPO的起始,但这主要发生在体外。细胞分离处理后的上清液中检测到高浓度的TBARS。我们观察到围手术期血红蛋白浓度和红细胞压积下降。术后,我们发现围手术期失血导致患者明显缺铁。没有足够的证据表明LPO的毒性代谢物会引起术后肝脏疾病。综上所述,在机器自体输血过程中,LPO产品对机体的污染程度很低。因此,诱导肝损伤似乎是不可能的。
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[Initiation of lipid peroxidation (LPO) in blood during intraoperative mechanical autotransfusion--is hepatotoxicity of lipid peroxidation products of clinical significance?].

Machine autotransfusion using cell-saver is a well-established method of saving homologous blood during extensive surgical procedures. The processing of blood may induce the initiation of lipid peroxidation (LPO) with the release of hepatotoxic products. A series of 42 patients undergoing primary (n = 20) or revision (n = 22) hip arthroplasty comprised the study group. Patients received an average of 1,260 ml of autologous blood and 2.2 units of homologous packed cells. The concentration of thiobarbituric acid reactive substances (TBARS) as LPO metabolites was measured in the patients' plasma, in the autologous packed cells as well as in the supernatants of the cell-saver-processed blood. Additionally, parameters of iron metabolism, haemoglobin levels, haematocrit as well as the activities of so-called liver enzymes aspartate aminotransferase, alanine aminotransferase, gamma-glutamyltranspeptidase and cholinesterase were determined. An initiation of LPO was detectable during the process of machine autotransfusion, but this took place mainly ex vivo. High concentrations of TBARS were detectable in the supernatants after cell-separation processing. We observed a decline in haemoglobin concentration and haematocrit during the perioperative period. Postoperatively, we found a significant iron deficiency as a consequence of the perioperative blood loss. There was not sufficient evidence of a postoperative liver disorder induced by toxic metabolites of LPO. To sum up, there is only a low contamination of the organism with LPO products during the process of machine autotransfusion. Therefore, an induction of liver damage seems to be improbable.

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