Department of Anaesthesia & Intensive Therapy, University of Pécs, Faculty of Medicine, Pécs, Hungary.
Indian J Med Res. 2011 Jul;134(1):69-78.
BACKGROUND & OBJECTIVES: We evaluated pro- and anti-oxidant disturbances in sepsis and non-sepsis burn patients with systemic inflammatory response syndrome (SIRS). Adhesion molecules and inflammation markers on leukocytes were also analyzed. We hypothesized that oxidative stress and leukocyte activation markers can lead to the severity of sepsis.
In 28 severe sepsis and 27 acute burn injury patients blood samples were collected at admission and 4 days consecutively. Oxidative stress markers: production of reactive oxygen species (ROS), myeloperoxidase, malondialdehyde and endogenous antioxidants: plasma protein sulphydryl groups, reduced glutathione, superoxide dismutase and catalase were measured. Flow cytometry was used to determine CD11a, CD14, CD18, CD49d and CD97 adhesion molecules on leukocytes. Procalcitonin, C-reactive protein, fibrinogen, platelet count and lactate were also analyzed.
Pro-oxidant parameters were significantly elevated in sepsis patients at admission, ROS intensity increased in burn patients until the 5th day. Endogenous antioxidant levels except catalase showed increased levels after burn trauma compared to sepsis. Elevated granulocyte activation and suppressed lymphocyte function were found at admission and early activation of granulocytes caused by increasing activation/migration markers in sepsis. Leukocyte adhesion molecule expression confirmed the suppressed lymphocyte and monocyte function in sepsis.
INTERPRETATION & CONCLUSIONS: Severe sepsis is accompanied by oxidative stress and pathological leukocyte endothelial cell interactions. The laboratory parameters used for the evaluation of sepsis and several markers of pro- and antioxidant status were different between sepsis and non-sepsis burn patients. The tendency of changes in these parameters may refer to major oxidative stress in sepsis and developing SIRS in burns.
我们评估了伴有全身炎症反应综合征（SIRS）的脓毒症和非脓毒症烧伤患者的促氧化剂和抗氧化剂紊乱。还分析了白细胞上的黏附分子和炎症标志物。我们假设氧化应激和白细胞活化标志物可导致脓毒症的严重程度。
在 28 例严重脓毒症和 27 例急性烧伤患者中，在入院时和连续 4 天采集血液样本。测定氧化应激标志物：活性氧（ROS）、髓过氧化物酶、丙二醛和内源性抗氧化剂：血浆蛋白巯基、还原型谷胱甘肽、超氧化物歧化酶和过氧化氢酶的产生。采用流式细胞术测定白细胞上的 CD11a、CD14、CD18、CD49d 和 CD97 黏附分子。还分析了降钙素原、C 反应蛋白、纤维蛋白原、血小板计数和乳酸。
脓毒症患者入院时促氧化剂参数显著升高，烧伤患者 ROS 强度直至第 5 天增加。与脓毒症相比，烧伤后除过氧化氢酶外，内源性抗氧化剂水平升高。入院时发现粒细胞活化升高和淋巴细胞功能抑制，以及脓毒症中由于激活/迁移标志物增加导致的粒细胞早期活化。白细胞黏附分子表达证实了脓毒症中淋巴细胞和单核细胞功能受抑制。
严重脓毒症伴有氧化应激和病理性白细胞内皮细胞相互作用。用于评估脓毒症的实验室参数以及促氧化剂和抗氧化剂状态的几种标志物在脓毒症和非脓毒症烧伤患者之间存在差异。这些参数变化的趋势可能表明脓毒症中存在较大的氧化应激和烧伤中 SIRS 的发展。
