Figure 2.

Pathogenesis of HIBI at the molecular level. Decreased cerebral perfusion impairs the function of Na⁺/K⁺ ATPase pump in the brain tissue due to decreased ATP production. This generates a hypoxic state which leads to a shift in metabolism from oxidative phosphorylation to anaerobic glycolysis. The resultant acidotic environment due to lactic acid accumulation impairs cell function. Furthermore, ischemia leads to an activation of NMDA receptor and influx of calcium ions. Calcium induces the release of excitotoxic neurotransmitter glutamate, which along with the reactive oxygen species and activation of degrative enzymes leads to neuronal cell death by necrosis, apoptosis, or autophagocytosis. This figure is created with the BioRender software, with the assistance of Soorin Chung in finalizing the graphic design.