Olanzapine-Induced Therapeutic Hypothermia Attenuates Renal Injury in Rats after Asphyxial Cardiac Arrest and Resuscitation

Return of spontaneous circulation (ROSC) through cardiopulmonary resuscitation (CPR) after cardiac arrest (CA) causes post-cardiac arrest syndrome (PCAS) due to dysfunction in various organs, which provokes acute kidney injury because of renal ischemia-reperfusion injury. Therapeutic hypothermia (TH...

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Bibliographic Details
Published in:Antioxidants 2022-02, Vol.11 (3), p.443
Main Authors: Tungalag, Tsendsuren, Yoo, Yeo-Jin, Tae, Hyun-Jin, Yang, Dong Kwon
Format: Article
Language:English
Subjects:
Antioxidants
Body temperature
Cardiac arrest
Cardiopulmonary resuscitation
Cerebral blood flow
CPR
Creatinine
Electrocardiography
Endoplasmic reticulum
FOXO3 protein
Heart
Hypothermia
Ischemia
ischemia–reperfusion injury
Kidneys
Methods
Mitochondria
Mortality
Neurological disorders
Olanzapine
Oxidative stress
Prevention
reactive oxygen species
Reperfusion
ROSC
Signal transduction
Sirt3
Stress response
Superoxide dismutase
Traumatic brain injury
Ventilation
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Summary:Return of spontaneous circulation (ROSC) through cardiopulmonary resuscitation (CPR) after cardiac arrest (CA) causes post-cardiac arrest syndrome (PCAS) due to dysfunction in various organs, which provokes acute kidney injury because of renal ischemia-reperfusion injury. Therapeutic hypothermia (TH) can reduce PCAS after CA and ROSC. However, it needs to be more sophisticated and effective. Hence, we aimed to elucidate the protective effects of olanzapine-induced TH against renal injury in asphyxial CA-induced rats. Every rat's body temperature was maintained at 33 °C for 6 h after administering olanzapine post-CA and ROSC. Olanzapine-induced TH dramatically increased the survival rate of the rats and ameliorated renal tissue damage. Moreover, it suppressed oxidative stress responses through preservation of mitochondrial function and endoplasmic reticulum stress as the main contributor of oxidative stress. Notably, these actions of olanzapine-induced TH were mediated through the Sirt3-related signaling pathway, including the maintenance of Sirt3 and FOXO3a protein expression and the activation of AMPKα and superoxide dismutase 1 (SOD2, a mitochondrial antioxidant). This study is the first to disclose the protective effects of olanzapine-induced TH against renal injury after CA and ROSC, suggesting that olanzapine-induced TH could be utilized for treating CA followed by ROSC.
ISSN:2076-3921
2076-3921
DOI:10.3390/antiox11030443