This is in agreement with preclinical work demonstrating increases in hippocampal IL-6 following cardiac arrest.44 IL-6 is produced by astrocytes (and other cells) in response to inflammation42 and may represent a key pathophysiological process of secondary hypoxic brain injury in humans with HIBI given the marked injury to astrocytes evidenced by the cerebral release of GFAP in the HIBI group with brain hypoxia. This evidence concerns the gene GFAP and cardiac arrest.