Transient Global Ischemia-Induced Brain Inflammatory Cascades Attenuated by Targeted Temperature Management

Sudden cardiac arrest leads to a significantly increased risk of severe neurological impairment and higher mortality rates in survivors due to global brain tissue injury caused by prolonged whole-body ischemia and reperfusion. The brain undergoes various deleterious cascading events. Among these dam...

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Bibliographic Details
Published in:International journal of molecular sciences 2021-05, Vol.22 (10), p.5114
Main Authors: Hong, Dae Ki, Park, Yoo Seok, Woo, Ji Sun, Kim, Ju Hee, Beom, Jin Ho, Chung, Sung Phil, You, Je Sung, Suh, Sang Won
Format: Article
Language:English
Subjects:
Apoptosis
Brain damage
Brain injury
Cardiac arrest
Cell activation
Cell death
Cerebral blood flow
Cytokines
Genotype & phenotype
Heart
high mobility box protein 1
Homeostasis
Hypothermia
Inflammation
Injuries
Ischemia
Microglia
Neurological complications
Neuroprotection
Polymerase chain reaction
post cardiac arrest care
Reperfusion
targeted temperature management
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Summary:Sudden cardiac arrest leads to a significantly increased risk of severe neurological impairment and higher mortality rates in survivors due to global brain tissue injury caused by prolonged whole-body ischemia and reperfusion. The brain undergoes various deleterious cascading events. Among these damaging mechanisms, neuroinflammation plays an especially crucial role in the exacerbation of brain damage. Clinical guidelines indicate that 33 °C and 36 °C are both beneficial for targeted temperature management (TTM) after cardiac arrest. To clarify the mechanistic relationship between TTM and inflammation in transient global ischemia (TGI) and determine whether 36 °C produces a neuroprotective effect comparable to 33 °C, we performed an experiment using a rat model. We found that TTM at 36 °C and at 33 °C attenuated neuronal cell death and apoptosis, with significant improvements in behavioral function that lasted for up to 72 h. TTM at 33 °C and 36 °C suppressed the propagation of inflammation including the release of high mobility group box 1 from damaged cells, the activation and polarization of the microglia, and the excessive release of activated microglia-induced inflammatory cytokines. There were equal neuroprotective effects for TTM at 36 °C and 33 °C. In addition, hypothermic complications and should be considered safe and effective after cardiac arrest.
ISSN:1422-0067
1661-6596
1422-0067
DOI:10.3390/ijms22105114