Decreased VEGF concentration in lung tissue and vascular injury during ARDS

Decreased VEGF concentration in lung tissue and vascular injury during ARDS
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DOI:
10.1183/09031936.04.00065504
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发表时间:
2005-01-01
影响因子:
24.3
通讯作者:
Delclaux, C
Delclaux, C
中科院分区:
医学1区
文献类型:
--
作者:
Abadie, Y;Bregeon, F;Delclaux, C

文献摘要

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内皮损伤是影响急性呼吸窘迫综合征(ARDS)预后的重要因素。ARDS患者血管内皮生长因子(VEGF)的减少可能有利于血管病变,因为VEGF通过抑制细胞凋亡促进内皮细胞存活。本研究旨在记录ARDS患者肺组织中低VEGF水平,以确定其原因是否为肺泡11型细胞(肺中VEGF的主要来源)损伤,并评估血管后果。29例严重急性呼吸窘迫综合征(ARDS)患者(2例幸存者)和5例对照患者通过开放性活检或尸检获得肺标本。与对照组相比,来自ARDS患者的肺组织匀浆液含有更少的VEGF(中位数(四分位数范围)ARDS 8.2(4.7-12.2)与对照组28.4 (9.9-47.1)ng (.) g(-1)蛋白)。肺表面活性蛋白B免疫染色增高。与对照组相比,ARDS肺中广泛的细胞凋亡(末端脱氧核苷酸转移酶介导的脱氧尿苷三磷酸镍端标记染色),包括内皮细胞和肺泡11型细胞,血管床密度(CD31免疫染色)下降。VEGF水平与凋亡内皮细胞计数呈负相关。综上所述,肺组织血管内皮生长因子水平降低可能参与了急性呼吸窘迫综合征肺灌注减少。
Endothelial injury is an important prognostic factor in acute respiratory distress syndrome (ARDS). Decreased production of vascular endothelial growth factor (VEGF) in ARDS may favour vascular lesions, since VEGF promotes endothelial survival by inhibiting apoptosis. This study sought to document low VEGF levels in lung tissue from ARDS patients, to determine whether the cause was injury to alveolar type 11 cells (the main pulmonary source of VEGF) and to evaluate the vascular consequences. Lung specimens were obtained by open biopsy or autopsy from 29 patients with severe ARDS (two survivors) and five controls.As compared with controls, homogenates of lung tissue from ARDS patients contained less VEGF (median (interquartile range) ARDS 8.2 (4.7-12.2) versus controls 28.4 (9.9-47.1) ng (.) g(-1) protein). Increased immunostaining with surfactant protein B was seen in ARDS lungs. Extensive cellular apoptosis (terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling staining), including endothelial and alveolar type 11 cells, was demonstrated, and vascular bed density (CD31 immunostaining) decreased in ARDS lungs as compared with controls. VEGF levels were negatively correlated to apoptotic endothelial cell counts.In conclusion, decreased vascular endothelial growth factor levels in lung tissue may participate in the decrease in lung perfusion in acute respiratory distress syndrome.