Intensive care unit, Special Hospital for Pulmonary Diseases, Zagreb, Croatia.
Eur Cytokine Netw. 2010 Jun;21(2):92-8. doi: 10.1684/ecn.2010.0193. Epub 2010 May 27.
Hypoxia frequently complicates the course of chronic obstructive pulmonary disease (COPD). Vascular endothelial growth factor (VEGF) and basic fibroblast growth factor (bFGF) are the two most potent angiogenic factors and may play a role in adaptation to hypoxia. The aims of the study were to assess the serum levels of VEGF and bFGF and to evaluate their mutual relationship in hypoxic patients with exacerbated COPD. The study group consisted of 50 hypoxic (PaO(2) 53 mmHg) patients with exacerbated COPD. Control groups were 30 stable COPD patients with PaO(2) 70 mmHg, and 30 healthy blood donors. The serum concentrations of VEGF and bFGF were measured using commercial enzyme-linked immunoassay kits. Patients with exacerbated COPD had significantly higher serum VEGF levels (1,089.16 +/- 1,128.03 pg/mL) compared to those with stable COPD (197.68 +/- 178.06 pg/mL) (p < 0.0001) and healthy blood donor group (257.69 +/- 170.4 pg/mL) (p < 0.0001). Serum bFGF levels were significantly higher in the exacerbated COPD group (6.15 +/- 2.56 pg/mL) compared to control groups (p = 0.0001). Basic FGF was undetectable in the stable COPD and blood donor groups. Since VEGF and bFGF correlated significantly with the majority of factors investigated in COPD patients, multivariate analysis was performed. According to the step-wise regression analysis, VEGF was best determined by PaO(2), WBC and IL-6. Basic FGF was best determined by PaO(2) and pH. The highly significant, simple correlation between VEGF and bFGF was lost in multivariate analysis. This suggests that their correlation is not independent, but due to factors that remain in the model after step-wise regression. These are essentially linked to the level of hypoxia. Results of our study suggest that VEGF and bFGF production is stimulated in hypoxic patients with exacerbated COPD. Elevated levels of VEGF and bFGF may activate the process of neoangiogenesis, which may lead to increased perfusion and an improvement in tissue oxygenation in this group of patients.
缺氧常使慢性阻塞性肺疾病(COPD)的病程复杂化。血管内皮生长因子(VEGF)和碱性成纤维细胞生长因子(bFGF)是两种最有效的血管生成因子,可能在适应缺氧中发挥作用。本研究的目的是评估 VEGF 和 bFGF 的血清水平,并评估它们在缺氧性 COPD 加重患者中的相互关系。研究组包括 50 例缺氧(PaO2 53mmHg)的 COPD 加重患者。对照组为 30 例 PaO2 70mmHg 的稳定 COPD 患者和 30 例健康献血者。使用商业酶联免疫吸附试剂盒测定血清 VEGF 和 bFGF 浓度。与稳定 COPD 患者(197.68 +/- 178.06pg/mL)(p <0.0001)和健康献血者组(257.69 +/- 170.4pg/mL)(p <0.0001)相比,COPD 加重患者的血清 VEGF 水平(1089.16 +/- 1128.03pg/mL)显著升高。与对照组相比,COPD 加重组的血清 bFGF 水平(6.15 +/- 2.56pg/mL)显著升高(p = 0.0001)。稳定 COPD 和献血者组中均未检测到 bFGF。由于 VEGF 和 bFGF 与 COPD 患者调查的大多数因素显著相关,因此进行了多变量分析。根据逐步回归分析,VEGF 由 PaO2、白细胞和 IL-6 最佳确定。bFGF 由 PaO2 和 pH 最佳确定。VEGF 和 bFGF 之间高度显著的简单相关性在多变量分析中丢失。这表明它们的相关性不是独立的,而是由于逐步回归后模型中存在的因素。这些因素基本上与缺氧水平有关。我们的研究结果表明,缺氧性 COPD 加重患者的 VEGF 和 bFGF 产生受到刺激。VEGF 和 bFGF 水平的升高可能激活新血管生成过程,从而导致该组患者的灌注增加和组织氧合改善。