Inhaled Gases as Therapies for Post–Cardiac Arrest Syndrome: A Narrative Review of Recent Developments

Frontiers in Medicine

Tai Yin¹  Koichiro Shinozaki¹  Kei Hayashida¹  Ryosuke Takegawa¹  Rishabh C. Choudhary¹  Sara Guevara³  Lance B. Becker⁴  Daniel M. Rolston⁴  Ernesto P. Molmenti⁴  Santiago J. Miyara⁶ 

[1] Department of Emergency Medicine, North Shore University Hospital, Northwell Health System, Manhasset, NY, United States;Department of Surgery, Medicine, and Pediatrics, Zucker School of Medicine at Hofstra/Northwell, New York, NY, United States;Department of Surgery, Northwell Health, Manhasset, NY, United States;Donald and Barbara Zucker School of Medicine at Hofstra/Northwell, Northwell Health, Hempstead, NY, United States;Elmezzi Graduate School of Molecular Medicine, Manhasset, NY, United States;Institute of Health Innovations and Outcomes Research, Feinstein Institutes for Medical Research, Northwell Health, Manhasset, NY, United States;Laboratory for Critical Care Physiology, Feinstein Institutes for Medical Research, Northwell Health System, Manhasset, NY, United States;

关键词: cardiac arrest;    cardiopulmonary resuscitation;    ischemia-reperfusion injury;    neuroprotection;    nitric oxide;    xenon;   

DOI  :  10.3389/fmed.2020.586229

来源: DOAJ

【 摘 要 】

Despite recent advances in the management of post–cardiac arrest syndrome (PCAS), the survival rate, without neurologic sequelae after resuscitation, remains very low. Whole-body ischemia, followed by reperfusion after cardiac arrest (CA), contributes to PCAS, for which established pharmaceutical interventions are still lacking. It has been shown that a number of different processes can ultimately lead to neuronal injury and cell death in the pathology of PCAS, including vasoconstriction, protein modification, impaired mitochondrial respiration, cell death signaling, inflammation, and excessive oxidative stress. Recently, the pathophysiological effects of inhaled gases including nitric oxide (NO), molecular hydrogen (H2), and xenon (Xe) have attracted much attention. Herein, we summarize recent literature on the application of NO, H2, and Xe for treating PCAS. Recent basic and clinical research has shown that these gases have cytoprotective effects against PCAS. Nevertheless, there are likely differences in the mechanisms by which these gases modulate reperfusion injury after CA. Further preclinical and clinical studies examining the combinations of standard post-CA care and inhaled gas treatment to prevent ischemia–reperfusion injury are warranted to improve outcomes in patients who are being failed by our current therapies.

【 授权许可】

Unknown