Morphological Changes in the Rat Brain in the Early Post-Resuscitation Period: The Relationship Between Hypoxia-Sensitive Immunohistochemical Markers, Hemodynamic and Acid–Base Status

The relevance of studying the molecular mechanisms of ischemia–reperfusion brain injury is due to the ongoing need to identify therapeutic targets to improve neurologic outcomes following cardiac arrest. This study aims to identify early morphological and molecular changes in the rat brain in the post-resuscitation period after asphyxial cardiac arrest, as well as to assess the relationship of these changes with hemodynamic and acid–base status. Morphological analysis using immunohistochemistry (IHC) revealed an increase in the intensity of the IHC reaction to S-100β protein in astrocytes of the hippocampal CA1 region in rats 3 hours after resuscitation compared to sham-operated controls (p = 0.043). Acid–base disturbances were associated with an increase in the intensity of microglia marker Iba-1 staining in the hippocampal CA4 region (p = 0.015). A correlation was found between the intensity of the IHC reaction to PHD1 in cortical neurons and the values of mean arterial pressure (r = −0.699, p < 0.001), PaO2/FiO2 ratio (r = −0.580, p < 0.005), PaCO2 (r = 0.507, p = 0.014). The results of this hypothesis-generating study suggest a potential association between the oxygen-sensing protein PHD1 in cerebral cortical neurons and clinically relevant indicators of post-resuscitation severity after cardiac arrest. Further studies are needed to clarify the role of oxygen-sensing prolyl hydroxylases in the pathogenesis of brain injury in critical illness accompanied by impaired central hemodynamics and acid–base imbalance.