The present study aimed to examine the effects of
hypoxia and cold on vascular endothelial cells (VECs), as well as the protective ability of novel VECs-
protective drugs against these
injuries. A rat model simulating exposure to
hypoxia and cold at high altitude environments was established. Based on these animal experiments, rat aortic VECs were established as injury models and exposed to
hypoxia and/or
adrenaline (ADR) in vitro. The results revealed that
hypoxia significantly altered the levels of
nitric oxide and
vascular endothelial growth factor, while the cold temperature significantly increased the release of ADR and
noradrenaline. Exposure to
hypoxia combined with cold temperature significantly affected all these indices. In vitro experiments demonstrated that
hypoxia, ADR (which was used to simulate cold in the animal experiments) and the combination of the two factors resulted in damage to the VECs and endothelial dysfunction. In addition, the results also showed that
diazoxide, a highly selective
mitoKATP opener, protected VECs against these
injuries. In conclusion,
hypoxia and cold temperature induced endothelial cell dysfunction and endocrine disorders, respectively. Improving endothelial function using
diazoxide may be an effective therapeutic strategy in patients with altitude-associated disorders. However, the potential for clinical application requires further study.