Preclinical studies suggest that nitric oxide inhalation therapy may improve neurological outcomes and survival in post-cardiac arrest syndrome, warranting future clinical trials.
Does nitric oxide inhalation therapy improve neurological outcomes and survival in post-cardiac arrest syndrome?
Preclinical evidence suggests that inhaled nitric oxide may improve survival and neurological outcomes in post-cardiac arrest syndrome, highlighting the need for clinical trials.
Sudden cardiac arrest is a leading cause of death worldwide. Although the methods of cardiopulmonary resuscitation have been improved, mortality is still unacceptably high, and many survivors suffer from lasting neurological deficits due to the post-cardiac arrest syndrome (PCAS). Pathophysiologically, generalized vascular endothelial dysfunction accompanied by platelet activation and systemic inflammation has been implicated in the pathogenesis of PCAS. Because endothelial-derived nitric oxide (NO) plays a central role in maintaining vascular homeostasis, the role of NO-dependent signaling has been a focus of the intense investigation. Recent preclinical studies showed that therapeutic interventions that increase vascular NO bioavailability may improve outcomes after cardiac arrest complicated with PCAS. In particular, NO inhalation therapy has been shown to improve neurological outcomes and survival in multiple species. Clinical studies examining the safety and efficacy of inhaled NO in patients sustaining PCAS are warranted.
Miyazaki et al. (Tue,) conducted a review in Post-cardiac arrest syndrome. Nitric Oxide inhalation therapy was evaluated. Preclinical studies suggest that nitric oxide inhalation therapy may improve neurological outcomes and survival in post-cardiac arrest syndrome, warranting future clinical trials.