Hypothermia and brain inflammation after cardiac arrest

Abstract

The cessation (ischemia) and restoration (reperfusion) of cerebral blood flow after cardiac arrest (CA) induce inflammatory processes that can result in additional brain injury. Therapeutic hypothermia (TH) has been proven as a brain protective strategy after CA. In this article, the underlying pathophysiology of ischemia-reperfusion brain injury with emphasis on the role of inflammatory mechanisms is reviewed. Potential targets for immunomodulatory treatments and relevant effects of TH are also discussed. Further studies are needed to delineate the complex pathophysiology and interactions among different components of immune response after CA and identify appropriate targets for clinical investigations.

Recent advances in personalizing cardiac arrest resuscitation

“…If the post-ischemic brain is unable to replenish PPL components because of metabolic derangement, direct administration of PPL precursors or other mitochondrial stabilizing agents such as SS-31 could be pursued to aid the brain in replenishing normal PPL composition. Furthermore, as brain tissue is less able to moderate pro-inflammatory LPLs after reperfusion, administration of anti-inflammatory medications or hypothermia 45 may be beneficial in reducing pro-inflammatory neuronal damage. Finally, as the brain appears to be uniquely sensitive to ROS damage, administration of free-radical scavenging compounds could provide additional benefit to the brain.…”

Effects of extracellular vesicles from mesenchymal stem cells on oxygen-glucose deprivation/reperfusion-induced neuronal injury

“…[3] These mechanisms intersect with each other, discounting the effect of any single pharmacotherapy, even comprehensive interventions (like hypothermia). [4,5] Therefore, it is urgent to fi nd a new, stable, and eff ective treatment. World J Emerg Med, Vol 12, No 1, 2021 Multipotent mesenchymal stem cells (MSCs) play a role in neurovascular remodeling and neurological recovery following cerebral ischemia injury.…”

Pharmacological Approach for Neuroprotection After Cardiac Arrest—A Narrative Review of Current Therapies and Future Neuroprotective Cocktail

“…Besides ACLS, there are limited evidence-based treatments that successfully improve survival and protect the brain after CA. The two major therapies used for treating CA that can aid in neuroprotection are extracorporeal cardiopulmonary resuscitation (E-CPR) and targeted temperature management (TTM); the former uses an external machine to oxygenate and circulate blood within the body (9), while the latter decreases and maintains the core temperature between 32 and 36 • C to decrease cellular metabolism, decrease oxidative damage and stress signals, and decrease cellular death (6,(10)(11)(12)(13). Although both E-CPR and TTM have therapeutic efficacy in CA patients, each has their limitations and can influence both protective and deleterious pathways (14).…”

“…Ischemia-reperfusion injury (IRI) begins with decreased perfusion to tissues, depletion of energetic substrates, and subsequent upregulation of the anaerobic metabolism ( 6 ). Under physiological conditions, the brain consumes 20% of the basal metabolic rate despite representing only 2% of the total body weight.…”