Attenuation of mitochondrial dysfunction in a ventricular fibrillation swine model of cardiac arrest treated with carbon monoxide.

ABSTRACT:

Background

Out-of-hospital cardiac arrest (OHCA) affects over 360,000 adults in the United States each year with a 50-80% mortality. Despite aggressive supportive care and use of targeted temperature management, half of adults do not live to hospital discharge and nearly one-third of survivors have significant neurologic injury. Development of neuroprotective therapeutics is critical to improving outcomes. One promising readily available agent that has shown benefit is carbon monoxide (CO).

Methods

We utilize a swine model of ventricular fibrillation (VF) arrest to assess the therapeutic effect of CO on cellular measures. All animals underwent VF arrest followed by cardiopulmonary resuscitation until achievement of return of spontaneous circulation (ROSC) or the 20 min mark.

SUBMITTER: Ko TS 

PROVIDER: S-EPMC12335330 | biostudies-literature | 2025 Aug

REPOSITORIES: biostudies-literature