Post-cardiac arrest brain injury: Pathophysiology and treatment

Making sense of clinical outcomes following cardiac arrest

“…A significant organ injury continues during the postresuscitation period (up to 72 h after ROSC) because of reperfusion injury and ongoing ischemia [43,44]. The impact of number of postresuscitation factors and interventions against these has been studied recently.…”

1H NMR-metabolomics: Can they be a useful tool in our understanding of cardiac arrest?

“…Nevertheless, mitochondria can kill neurons by releasing apoptotic factors into cytosol, by releasing Ca 2+ , and/or by generating ROS. 11 Meanwhile, disturbances in Ca 2+ homeostasis, inhibition of glycolysis, and oxidative stress triggers the release of signaling proteins and the activation of apoptotic mechanisms, such as the apoptotic pathway of stress-activated protein kinases (SAPKs) 1 and 2. 12,13 Also, MTP opening can lead to apoptosis via cytochrome c release and/or may promote autophagy, 14 while apoptosis may be also initiated by hypoxia-induced p53 accumulation which, in turn, it directly interacts with HIF 1-a and limits its expression.…”

“…19 Despite the fact that ROSC is characterized by the upregulation and release of several cytokines and especially TNF-a and IL-8, 20 targeted temperature management suppresses the production of proinflammatory cytokines and may block other manifestations associated with post-cardiac arrest syndrome, such as the increase of intracellular Ca 2+ and glutamate which is observed after exposure to excitotoxin. 11 The chemical changes that occur during cardiac arrest predispose to a massive burst of ROS production during the first minutes after ROSC, although free-radical production and vascular permeability may be attenuated by induced hypothermia. 21 The endothelium becomes more dysfunctional and NO formation decreases, resulting in impaired vasodilation, further activation of PMN and platelets and extend tissue injury.…”

Effects of Ghrelin on Postresuscitation Brain Injury in a Rat Model of Cardiac Arrest

“…This injury cascade begins with ischemia and reperfusion (I/R), but it can continue for hours to days and finally lead to neuronal necrosis and apoptosis in vulnerable areas (5). To date, therapeutic hypothermia is regarded as the only effective treatment for postresuscitation brain injury, but even it has not yet been shown to lead to a high level of neurological function recovery (2).…”