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.