Type 1 respiratory failure-induced hypoxemia causes hypoxia and apoptosis and triggers complex signaling pathways in the rat brain

Type 1 respiratory failure (T1RF) is associated with secondary acute brain injury (sABI), but the mechanisms behind it are not clear and could include primary hypoxic injury, increased intracranial pressure, or could be mediated by lung injury-triggered inflammation. This study aimed to elucidate the effects of T1RF-induced hypoxemia on the brain in the absence of lung injury. <br> These data show results of the study in which SD rats were exposed to 8%O2 in N2 for up to 48h. Tissue PO2 (PtO2), cerebral blood flow (CBF) and lactate concentration in the cerebral cortex (CC) were measured and apoptosis in the CC, ependymal layer (EL) and choroid plexuses (CPs) was estimated using the TUNEL assay. Cerebrospinal fluid (CSF) samples were collected at various time points and the concentrations of 32 signaling molecules were estimated in these samples by multiplex assays. Expressions of 84 signaling molecules and 5 housekeeping genes in the CC were explored by RT2 ProfilerTM PCR Array. Values are presented as mean (SD). Data was compared with one-way ANOVA and the Kruskal-Wallis test. The Mann-Kendall test was used to assess whether CBF was increasing or decreasing during hypoxemia. Fold changes in the expressions of the tested mRNAs were estimated using GeneGlobe software. Statistical significance was set at p&lt;0.05.