Department for Medical Biochemistry, Faculty of Pharmacy, University of Belgrade, Belgrade, Serbia.
Respir Med. 2011 Oct;105 Suppl 1:S31-7. doi: 10.1016/S0954-6111(11)70008-7.
Oxidative stress and inflammation play an important role in the pathogenesis of chronic obstructive pulmonary disease (COPD).
Pulmonary function, oxidative stress parameters and inflammatory markers were measured in 74 patients with severe COPD exacerbation and 41 healthy subjects. In patients all parameters were assessed at two time points: Firstly, one day after admission and secondly, after 7 10 days when they were clinically stable enough to be discharged. Patients were divided in two groups according the presence of ischemic heart disease (IHD): IHD positive (IHD+) patients and IHD negative (IHD-) patients.
During hospitalisation O2•-, malondialdehyde (MDA), advanced oxidation protein products (AOPP) and total oxidant status (TOS) increased and were higher at discharge compared with admission and the control group. Superoxide dismutase (SOD) activity was significantly lower in COPD patients at both time points compared with the control group. Total antioxidant status (TAS) was significantly lower and the prooxidant-antioxidant balance (PAB) was higher at both time points in COPD patients compared with the control group. High sensitive C-reactive protein (hsCRP) and also the neutrophil count were significantly higher at admission compared with discharge. Paraoxonase 1 (PON1) enzymatic activities in COPD patients did not differ compared with the control group. IHD+ COPD patients had significantly lower PON1 activity but higher PAB levels and hsCRP concentrations, compared with IHD COPD patients.
The oxidant/antioxidant imbalance was significantly pronounced in patients with COPD exacerbation for at least 24 hours following their admission and when they were clinically stable enough to be discharged. Increased oxidative stress, elevated systemic inflammation and decreased antioxidant defence were common in end-stage disease and particularly COPD patients with ischemic heart disease.
氧化应激和炎症在慢性阻塞性肺疾病（COPD）的发病机制中起着重要作用。
测量 74 例重度 COPD 加重患者和 41 例健康受试者的肺功能、氧化应激参数和炎症标志物。在患者中，所有参数均在两个时间点进行评估：首先，入院后一天，其次，在临床稳定足以出院的 7-10 天后。根据是否存在缺血性心脏病（IHD），将患者分为两组：IHD 阳性（IHD+）患者和 IHD 阴性（IHD-）患者。
住院期间，O2•-、丙二醛（MDA）、高级氧化蛋白产物（AOPP）和总氧化状态（TOS）增加，出院时高于入院时和对照组。与对照组相比，COPD 患者在两个时间点的超氧化物歧化酶（SOD）活性均显著降低。COPD 患者在两个时间点的总抗氧化状态（TAS）均显著降低，促氧化剂-抗氧化剂平衡（PAB）均高于对照组。入院时高敏 C 反应蛋白（hsCRP）和中性粒细胞计数均明显高于出院时。与对照组相比，COPD 患者的对氧磷酶 1（PON1）酶活性没有差异。与 IHD COPD 患者相比，IHD+COPD 患者的 PON1 活性显著降低，但 PAB 水平和 hsCRP 浓度更高。
至少在入院后 24 小时，当 COPD 患者临床稳定足以出院时，COPD 加重患者的氧化应激/抗氧化失衡明显明显。在终末期疾病中，特别是在伴有缺血性心脏病的 COPD 患者中，氧化应激增加、全身炎症升高和抗氧化防御能力降低是常见的。
