Hyperbaric Oxygen Attenuates Cerebral Ischemia-Reperfusion Injury in Rats by Modulating Sodium Channels.

Abstract

Ischemic stroke accounts for the majority of stroke cases. Hyperbaric oxygen therapy (HBOT) is being increasingly used as a treatment for this condition, but its precise mechanisms of action remain incompletely elucidated. This study examined hyperbaric oxygen (HBO) effects on sodium channels in hippocampal CA1 pyramidal neurons in rats with cerebral ischemia-reperfusion injury (CIRI). Using the middle cerebral artery occlusion (MCAO) model and whole-cell patch-clamp technology, voltage-gated sodium channel (VGSC) currents were measured at varying HBOT time points and treatment durations. Results showed that with a longer CIRI duration, the maximum current density (MCD) of sodium current (INa) decreased, while more HBOT sessions increased the MCD of INa. Notably, in the MCAO 6H group, 12 treatments of HBOT induced a leftward shift in the INa activation curve. Early HBOT intervention provided greater neuroprotection for sodium channels, and increased treatment sessions enhanced functional recovery. These findings suggest HBO's therapeutic potential in mitigating CIRI-related neuronal damage.