Mancuso Patrizia, Peccatori Fedro, Rocca Andrea, Calleri Angelica, Antoniotti Pierluigi, Rabascio Cristina, Saronni Luca, Zorzino Laura, Sandri Maria Teresa, Zubani Anna, Bertolini Francesco
Division of Hematology-Oncology, European Institute of Oncology, Milan, Italy.
Endothelium. 2008 Jan-Feb;15(1):53-8. doi: 10.1080/10623320802092344.
High altitude and hypoxia are known to induce polycythemia, pulmonary hypertension, and vascular remodeling. The authors investigated a number of blood cell populations in 15 mountain trekkers before and after 12 days spent at >3000 m. Red blood cell and platelet count increased, whereas circulating hematopoietic stem cell (enumerated as CD34bright cells), circulating endothelial cell (CEC) and circulating endothelial progenitor (CEP) count significantly decreased. In particular, the authors observed a decrease in the count of viable CECs, and a decrease in the circulating levels of RNA of the endothelial-specific gene VE-cadherin, whereas the fraction of apoptotic/necrotic CECs was stable. These data suggest a unique pattern of modulation of surrogate markers of vascular remodeling induced by exposure to hypobaric hypoxia.
众所周知，高海拔和低氧会导致红细胞增多症、肺动脉高压和血管重塑。作者对15名登山者在海拔>3000米处停留12天前后的多个血细胞群体进行了研究。红细胞和血小板计数增加，而循环造血干细胞（以CD34bright细胞计数）、循环内皮细胞（CEC）和循环内皮祖细胞（CEP）计数显著减少。特别是，作者观察到存活CEC数量减少，内皮特异性基因VE-钙黏蛋白的RNA循环水平降低，而凋亡/坏死CEC的比例稳定。这些数据表明，暴露于低压低氧环境会导致血管重塑替代标志物出现独特的调节模式。
