Abstract
Sudden cardiac arrest is a leading cause of death worldwide [1]. Despite advances in cardiopulmonary resuscitation (CPR) methods, including the introduction of the automatic electrical defibrillator (AED) and therapeutic hypothermia [2, 3], only about 10 % of adult out-of-hospital cardiac arrest (OHCA) victims survive to hospital discharge [4], and the majority of survivors have moderate to severe cognitive deficits 3 months after resuscitation [5]. Resuscitation from cardiac arrest is the ultimate whole body ischemia-reperfusion (I/R) injury affecting multiple organ systems including brain and heart [6]. No pharmacological agent is available to improve outcome from post-cardiac arrest syndrome.
Highlights
Sudden cardiac arrest is a leading cause of death worldwide [1]
Despite advances in cardiopulmonary resuscitation (CPR) methods, including the introduction of the automatic electrical defibrillator (AED) and therapeutic hypothermia [2], [3], only about 10 % of adult out-of-hospital cardiac arrest (OHCA) victims survive to hospital discharge [4], and the majority of survivors have moderate to severe cognitive deficits 3 months after resuscitation [5]
Whether inhaled nitric oxide (NO) combined with therapeutic hypothermia further improves outcomes after cardiac arrest/CPR compared to mice treated with therapeutic hypothermia alone remains to be formally determined in future studies
Summary
Sudden cardiac arrest is a leading cause of death worldwide [1]. Despite advances in cardiopulmonary resuscitation (CPR) methods, including the introduction of the automatic electrical defibrillator (AED) and therapeutic hypothermia [2], [3], only about 10 % of adult out-of-hospital cardiac arrest (OHCA) victims survive to hospital discharge [4], and the majority of survivors have moderate to severe cognitive deficits 3 months after resuscitation [5]. Observations in rodents have been extended to a clinically-relevant porcine model of cardiac I/R injury: Liu and colleagues reported that, in pigs subjected to 50 min of cardiac ischemia and 4 h of reperfusion, breathing 80 ppm NO decreased MI size and improved myocardial perfusion [41] Taken together, these observations suggest that inhaled NO exerts beneficial effects on I/R and protects extrapulmonary organs from I/R injury in small and large mammals. Mathru and colleagues reported that breathing 80 ppm NO reduced I/R induced inflammatory injury in patients undergoing knee surgery [45] Based on these observations, we hypothesized that NO inhalation could improve outcomes after cardiac arrest/CPR
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