ABSTARCT
Background and Purpose
Brain injury is the main cause of high mortality and disability after successful cardiopulmonary resuscitation (CPR) from sudden cardiac arrest (CA). Transient receptor potential M4 (TRPM4) channel is a novel target for ameliorating blood-brain barrier (BBB) disruption and neuroinflammation. Herein, we tested whether flufenamic acid (FFA), which is reported to block TRPM4 with high potency, confers neuroprotection against brain injury secondary to CA/CPR and whether the action is exerted by blocking the TRPM4 channel.