BACKGROUND: Hypoxemia can cause secondary acute brain injury, but the mechanisms behind it are not entirely clear and could involve disturbances in the brain extracellular fluids. We aimed to explore the effects of hypoxemia on the choroid plexus (CPs) and cerebrospinal fluid (CSF) system in rats. METHODS: Male Sprague Dawley rats were kept in O RESULTS: Duration of hypoxemia exerted significant effects on the cell viability in the CPs (p <
0.01) and EL (p <
0.01) and caused apoptosis-related changes in the CP. Hypoxemia had significant effects on the protein concentration in the CSF (p <
0.05), but not in plasma (p >
0.05), with a significant increase in the CSF albumin-to-total protein ratio after 6 h hypoxemia (p <
0.05). Thirty-two cytokines were detected in the CSF. Hypoxemia caused a statistically significant reduction in the concentrations of 12 cytokines, while concentrations of erythropoietin (EPO) and vascular endothelial growth factor (VEGF) increased significantly. Exposure to hypoxemia after inhibitions of EPO, VEGF, or tumor necrosis factor alpha (TNFα) signaling resulted in more dead cells (p <
0.01), less dead cells (p <
0.01) and more dead cells (p <
0.01) in the CPs, respectively, when compared to the number of dead cells when these cytokines were not inhibited. The density of macrophages in the CPs decreased significantly during hypoxemia
that effect was cancelled out by TNFα inhibition. CONCLUSION: Hypoxemia had detrimental effects on the CPs and CSF system, which was modulated by hypoxia- and inflammation-related cytokines.