Pfeifer M, Blumberg F C, Wolf K, Sandner P, Elsner D, Riegger G A, Kurtz A
Klinik und Poliklinik für Innere Medizin II, University of Regensburg, Germany.
Respir Physiol. 1998 Feb;111(2):201-12. doi: 10.1016/s0034-5687(97)00102-3.
Recent studies suggest that the vasoactive peptides endothelin-1 and -3 and the mitogens VEGF and PDGF-A and -B could be involved in the pathogenesis of hypoxic pulmonary hypertension. We were interested to investigate whether these peptides could also be involved in the vascular remodeling occurring during chronic hypoxia (10% oxygen; 1 and 3 weeks) in the rat. Hypoxia increased significantly systolic right ventricular pressure and typical morphological signs of vascular remodeling were found. This was accompanied by increased ET-1 and the ET-3 mRNA expression after acute (6 h; P < 0.05) and chronic hypoxia of 1 (P < 0.05) and 3 weeks (P < 0.05). In contrast, we found no effects of hypoxia on the gene expression of VEGF and PDGF-A and -B in the lung. Our findings indicate that ET-3 in addition to ET-1 could be involved in the process of hypoxia-induced vascular remodeling, whereas it appears less likely that the mitogens VEGF and PDGF-A and -B are essentially involved in the pathogenesis of hypoxic pulmonary hypertension.
近期研究表明，血管活性肽内皮素-1和-3以及促细胞分裂剂血管内皮生长因子（VEGF）、血小板衍生生长因子-A（PDGF-A）和-B可能参与了缺氧性肺动脉高压的发病机制。我们感兴趣的是研究这些肽是否也参与大鼠慢性缺氧（10%氧气；1周和3周）过程中发生的血管重塑。缺氧显著增加了收缩期右心室压力，并发现了血管重塑的典型形态学特征。这伴随着急性缺氧（6小时；P<0.05）以及1周（P<0.05）和3周（P<0.05）慢性缺氧后内皮素-1和内皮素-3信使核糖核酸（mRNA）表达增加。相比之下，我们发现缺氧对肺中血管内皮生长因子、血小板衍生生长因子-A和-B的基因表达没有影响。我们的研究结果表明，除内皮素-1外，内皮素-3可能参与缺氧诱导的血管重塑过程，而促细胞分裂剂血管内皮生长因子、血小板衍生生长因子-A和-B似乎不太可能在缺氧性肺动脉高压的发病机制中起主要作用。
