Lin Y, et al. The American Journal of Emergency Medicine, 2024, 78, 48-56.
The study indicates that early administration of sodium octanoate can significantly alleviate cardiac and cerebral injuries following traumatic cardiac arrest (TCA) by inhibiting apoptosis and ferroptosis. These findings suggest that sodium octanoate could offer a novel therapeutic approach for improving outcomes in TCA patients by protecting against post-resuscitation damage.
Methods: The study utilized 22 male domestic pigs, divided into three groups: Sham (n = 7), TCA (n = 7), and sodium octanoate (SO) (n = 8). TCA was induced by hemorrhage via the right femoral artery. The Sham group underwent endotracheal intubation and catheterization without blood loss or resuscitation. Five minutes post-resuscitation, the SO group received a continuous infusion of sodium octanoate, while the TCA group received saline. Biomarkers for cardiac and cerebral injury were monitored at baseline and various time points, and samples of heart and brain tissues were analyzed for apoptosis, iron deposition, oxidative stress, and ferroptosis-related protein expression (ACSL4 and GPX4).
Results: Sodium octanoate infusion significantly improved mean arterial pressure, cardiac output, and ejection fraction post-TCA. The SO group exhibited lower levels of serum biomarkers indicative of cardiac and cerebral injury compared to the TCA group. Furthermore, sodium octanoate reduced apoptosis rates in cardiomyocytes and cerebral cortex cells and decreased iron deposition and oxidative stress. It also downregulated ferroptosis by modulating ACSL4 and GPX4 protein levels.