航天飞行后的立位耐力不良现象严重影响飞行安全与飞行人员健康，动脉结构与功能重塑是重要原因之一，其发生机制尚不清晰。酸性鞘磷脂酶（acid sphingomyelinase, ASM）可水解膜鞘磷脂产生神经酰胺(ceramide, Cer)，进而通过活性氧（redox oxygen species, ROS）及炎性反应等机制导致包括动脉的多种组织功能障碍与结构改变。失重所致血流动力学和血液内环境变化可激活动脉ASM/Cer通路。我们前期研究发现模拟失重大鼠颈总动脉ASM活性及Cer含量显著增高，介导动脉ROS生成和功能改变。推测“模拟失重可激活动脉ASM/Cer引发局部ROS产生和炎性反应导致其结构与功能重塑”。本课题拟在尾部悬吊模拟失重大鼠中，继续深入阐明不同动脉ASM/Cer改变在其结构与功能变化中的作用及下游机制。所得结论将为飞行后立位耐力不良机制理论及载人航天医务保障提出新的建议。

Orthostatic intolerence following spaceflight threaten the flight safety and health of astronauts in which the structural and functional remodeling of arteries plays an essential role, but the mechanisms of its happening are still unclear. The activation of acid sphingomyelinase (ASM) could hydrolyze sphingomyeline to produce ceramide (Cer) promoting dysfunction and structural variation in multiple tissues through pathways as redox oxygen species (ROS) formation and inflammation. The alteration of hemodynamics and blood hemostasis during weightlessness may promote the activation of ASM/Cer in arteries. The results of our original research have shown that the protein abundance and activity of ASM in carotid artery of simulated weightless rats were enhanced significantly and the Cer had a higher content and aggregration status which mediated the ROS production and changes of vasocontractile response of the artery. In the study, we will keep clarifying the modification of ASM/Cer pathway in arteries of tail suspended rat which is a internationally acknowledged weightless animal model. The objective is to tesify the hypotheiss that the simulated weightlessness activates ASM/Cer inducing ROS production and inflammation to cause the remodeling of both stucture and function in arteries. Our result might raise new viewpoint and suggestions to the research on mechanisms of orthostatic intolerence and medical protection during manned space flight.