Therapeutic Hypothermia: Critical Review of the Molecular Mechanisms of Action

Abstract

Therapeutic hypothermia (TH) is nowadays one of the most important methods of neuroprotection. The events that occur after an episode of ischemia are multiple and hypothermia can affect the various steps of this cascade. The mechanisms of action of TH are varied and the possible explanation for the benefits of this therapy is probably the multiple mechanisms of action blocking the cascade of ischemia on many levels. TH can affect many metabolic pathways, reactions of inflammation, apoptosis processes, and promote neuronal integrity. To know the mechanisms of action of TH will allow a better understanding about the indications for this therapy and the possibility of searching for other therapies when used in conjunction with hypothermia will provide a therapeutic synergistic effect.

Advances in Resuscitation

“…The preponderance of evidence comes from neuroscience research and includes evidence for reductions in excitatory neurotransmitters, inflammatory cytokines, leukotrienes, free radicals, and inflammatory cells; inhibition of apoptotic neuronal cell death; promotion of neuroprotective growth factors; reduced brain metabolic demand; and suppression of epileptogenic electric activity. 115 The strongest indication for TH is in patients after cardiac arrest resulting 18 from ventricular fibrillation, an indication that was supported by the original reports on TH published in 2002. 116,117 Subsequent work has confirmed beneficial outcomes in postventricular fibrillation cardiac arrest patients and in patients associated with any arrest rhythm.…”

Clinical neurorestorative progresses in cerebral palsy

“…50 Using hypothermia in combination with other therapies such as cell therapy, erythropoietin, and helium may be more beneficial to tackle the activated cell death pathways. 51 …”

İnme ve Terapötik Hipotermi

“…Serbest radikal ve lökotrienler gibi sitotoksik ürünler geri dönüşümsüz mitokondriyal hasara yol açar. İnflamasyon, apopitoz ve nekroz, intraselüler Ca⁺ 2 artışıyla tetiklenir [34][35][36] .…”