Flufenamic acid improves survival and neurologic outcome after successful cardiopulmonary resuscitation in mice.

ABSTRACT:

Background

Brain injury is the main cause of high mortality and disability after successful cardiopulmonary resuscitation (CPR) from sudden cardiac arrest (CA). The 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, could confer neuroprotection against brain injury secondary to CA/CPR and whether its action was exerted by blocking the TRPM4 channel.

Methods

Wild-type (WT) and Trpm4 knockout (Trpm4^-/-) mice subjected to 10-min CA/CPR were randomized to receive FFA or vehicle once daily. Post-CA/CPR brain injuries including neurologic deficits, survival rate, histological dama

SUBMITTER: Chen J 

PROVIDER: S-EPMC9438280 | biostudies-literature | 2022 Sep

REPOSITORIES: biostudies-literature