Department of Anesthesiology and Intensive Care Medicine, University Hospital Giessen and Marburg, Giessen, Germany.
J Surg Res. 2011 Jun 15;168(2):243-52. doi: 10.1016/j.jss.2009.10.028. Epub 2009 Nov 11.
Lipid peroxidation processes (LPO) are evident in many organ failures. Due to their toxic properties, they are causative for cellular dysfunction at the site of their origin and far beyond. This study was conducted to investigate differences in LPO pattern of patients with established acute respiratory distress syndrome (ARDS) and patients with end-stage liver failure undergoing liver transplantation (LTX) as two mayor prototypes of organ failure.
In this prospective, nonrandomized, controlled trial, we examined LPO by measuring malondialdehyde (MDA), and the volatile aldehydes hexanal and propanal as LPO-markers. Eighteen patients with ARDS, 16 subjects undergoing liver transplantation due to liver failure, and 8 healthy controls were included to the study.
ARDS patients showed significantly higher levels in MDA concentrations than LTX and controls, respectively. However, MDA levels of patients with end-stage liver failure were equal to those of controls. Blood concentrations of hexanal and propanal, specific by-products of lipid peroxidation, were elevated in both patient groups, but significantly higher only in LTX. Unexpectedly, hexanal and propanal concentrations were significantly higher in LTX than in ARDS patients. In both patient groups, MDA showed no differences between arterial and mixed venous blood, whereas volatile aldehydes were higher in arterial than in mixed venous compartment.
Both ARDS and LTX-patients showed significant evidence of enhanced LPO. However, proportions of MDA and volatile aldehydes differed substantially between the groups. Thus, for the interpretation of LPO markers, disease-specific factors have to be taken into account. Distinctions might be attributable to differences in the effected lipid components or variations in metabolism.
脂质过氧化过程（LPO）在许多器官衰竭中都很明显。由于其毒性，它们是起源部位和远处细胞功能障碍的原因。本研究旨在研究已确诊的急性呼吸窘迫综合征（ARDS）患者和接受肝移植（LTX）的终末期肝功能衰竭患者的 LPO 模式差异，这两种都是器官衰竭的主要原型。
在这项前瞻性、非随机、对照试验中，我们通过测量丙二醛（MDA）以及挥发性醛类己醛和丙醛作为 LPO 标志物来检查 LPO。共纳入 18 例 ARDS 患者、16 例因肝功能衰竭接受肝移植的患者和 8 例健康对照者。
ARDS 患者的 MDA 浓度明显高于 LTX 和对照组。然而，终末期肝功能衰竭患者的 MDA 水平与对照组相当。两种患者组的血液中己醛和丙醛浓度均升高，这是脂质过氧化的特定副产物，但仅在 LTX 中升高更为显著。出乎意料的是，LTX 患者的己醛和丙醛浓度明显高于 ARDS 患者。在两组患者中，MDA 在动脉血和混合静脉血之间无差异，而挥发性醛类在动脉血中的浓度高于混合静脉血。
ARDS 和 LTX 患者均显示出明显的 LPO 增强证据。然而，MDA 和挥发性醛类的比例在两组之间有很大差异。因此，对于 LPO 标志物的解释，必须考虑疾病特异性因素。差异可能归因于受影响的脂质成分的差异或代谢的变化。
