The role of hyperbaric oxygen in treating brain dysfunction and promoting brain resuscitation after CPR: 1. The role of hyperbaric oxygen in promoting wakefulness: HBO increases vertebral artery blood flow by 18%, increases the partial pressure of oxygen in the brainstem reticular system, promotes the establishment of collateral circulation and brain cell regeneration and repair, facilitates the improvement of waking state and promotes the recovery of consciousness and wakefulness. 2.Hyperbaric oxygen can reduce the intracranial pressure: the cerebral blood flow is reduced by 21% and the intracranial pressure is reduced by 36% in 2ATA; the cerebral blood flow is reduced by 25% and the intracranial pressure is reduced by 40%-50% in 3ATA. Therefore, hyperbaric oxygen can interrupt the vicious circle of cerebral hypoxia and cerebral edema. 3, hyperbaric oxygen increases oxygen content: HBO treatment increases oxygen content and may prevent brain tissue ischemia in patients with cardiac arrest syndrome. 25 minutes of cardiac arrest in experimental pigs resuscitated by applying 4.0 ATA HBO treatment can show a sustained ROSC state, a result not obtained in experimental pigs with normal oxygen pressure. 4, hyperbaric oxygen can reduce apoptosis and promote neural regeneration: HBO can promote central oxygenation, reduce blood-brain barrier permeability, reduce inflammatory response, reduce metabolic disorders, reduce apoptosis and increase neural regeneration; HBO can correct cardiac arrest, the decline in central oxygen uptake rate after resuscitation and the rapid rise in peak afterwards, thus playing a role in inhibiting neural death after resuscitation and promoting neural prognosis. 5.Hyperbaric oxygen improves cerebral aerobic metabolism: HBO promotes recovery of damaged mitochondria, preserves mitochondrial integrity, improves cerebral aerobic metabolism from the cellular level, and thus plays a neuroprotective role. HBO therapy has been shown to improve brain injury in various animal models. At the molecular level, HBO treatment activates ion channels and inhibits hypoxia-inducible factor α1 and its target genes, thereby reducing the increase in blood-brain barrier permeability and protecting brain tissue; it increases Bcl-2 and inhibits MMP-9 (matrix metalloproteinase-9) expression to protect brain tissue around the lesion from secondary damage and protect brain function. Combining both the antioxidant and pro-oxidant enzyme activities of hyperbaric oxygen seems to be a reasonable explanation for its inhibition of neuronal cell death and neurological damage induced after central ischemia.