研究表明，航天失重致动脉血管结构和功能的重建是宇航员返地后发生立位耐力不良的主要原因。然，其中涉及的详细机理，目前尚未完全阐明。血管细胞糖萼是位于细胞表面的一层多糖蛋白复合结构，更是细胞表面重要的力感受器。申请人研究发现，模拟失重将引起大鼠动脉血管内皮细胞糖萼在厚度上发生区域性重塑，证实了糖萼对于模拟失重环境的敏感性。在此基础上，本课题设计了5个方面的研究内容来验证申请人的2个科学猜想：1）除厚度外，模拟失重可能引发动脉血管糖萼在覆盖率及组成成分的表达水平上发生区域性重塑。2）作为力感受器，糖萼的这种重塑很可能会影响下游NO等信号分子的释放，NOS及SMC收缩蛋白的表达，以及SMC的增殖/凋亡，最终改变动脉的舒缩能力，参与模拟失重致动脉血管功能重建的过程。本课题的实施，将有望从一个新的角度去解释宇航员返地后立位耐力不良的发生机理，并为以糖萼为靶点，寻求新的对抗措施提供理论依据。

Recent studies have revealed that microgravity induced vascular structural and functional remodeling may be one of the key contributors to postspaceflight orthostatic intolerance experienced by astronauts on return to Earth. Nevertheless, the mechanisms underneath remain unclear. The vascular cell (endothelial cell and smooth muscle cell) glycocalyx is a surface layer mainly composed of glycosaminoglycans and its bearing core proteins, and also a key mechaosensor. The applicant’s previous study has demonstrated that simulated microgravity induces the vascular endothelial glycocalyx dimensional remodeling in a regional-dependent manner, which suggests the sensitivity of the glycocalyx to the redistribution of the hemodynamic environments in tail-suspended rats. Based on this, the applicant proposed this research project to testify the following 2 hypothesis: 1) Not only the thickness but also the coverage and the expression levels of glycocalyx will be modulated by simulated microgravity in tail-suspended rats. 2) As a mechanosensor, the adaptation of the glycocalyx may affect the release of nitric oxide (NO), the expression levels of nitric oxide synthase (NOS) and smooth muscle cell (SMC) markers, and the proliferation or apoptosis of SMC, consequently, alter the contractility of the artery, contributing to the vascular functional remodeling in tail-suspended rats. The proposed research project can enrich our understanding of orthostatic intolerance of astronauts on return to Earth and provide theoretical basis to seek potential countermeasures in the future.