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Therapeutic hypothermia reduces inflammation and oxidative stress in the liver after asphyxial cardiac arrest in rats
Yoonsoo Park, Ji Hyeon Ahn, Tae-Kyeong Lee, Bora Kim, Hyun-Jin Tae, Joon Ha Park, Myoung Cheol Shin, Jun Hwi Cho, Moo-Ho Won
Acute Crit Care. 2020;35(4):286-295.   Published online November 30, 2020
DOI: https://doi.org/10.4266/acc.2020.00304
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  • 5 Web of Science
  • 7 Crossref
AbstractAbstract PDF
Background
Few studies have evaluated the effects of hypothermia on cardiac arrest (CA)-induced liver damage. This study aimed to investigate the effects of hypothermic therapy on the liver in a rat model of asphyxial cardiac arrest (ACA).
Methods
Rats were subjected to 5-minute ACA followed by return of spontaneous circulation (RoSC). Body temperature was controlled at 33°C±0.5°C or 37°C±0.5°C for 4 hours after RoSC in the hypothermia group and normothermia group, respectively. Liver tissues in each group were collected at 6 hours, 12 hours, 1 day, and 2 days after RoSC. To examine hepatic inflammation, mast cells were stained with toluidine blue. Superoxide anion radical production was evaluated using dihydroethidium fluorescence straining and expression of endogenous antioxidants (superoxide dismutase 1 [SOD1] and SOD2) was examined using immunohistochemistry.
Results
There were significantly more mast cells in the livers of the normothermia group with ACA than in the hypothermia group with ACA. Gradual increase in superoxide anion radical production was found with time in the normothermia group with ACA, but production was significantly suppressed in the hypothermia group with ACA relative to the normothermia group with ACA. SOD1 and SOD2 levels were higher in the hypothermia group with ACA than in the normothermia group with ACA.
Conclusions
Experimental hypothermic treatment after ACA significantly inhibited inflammation and superoxide anion radical production in the rat liver, indicating that this treatment enhanced or maintained expression of antioxidants. Our findings suggest that hypothermic therapy after CA can reduce mast cell-mediated inflammation through regulation of oxidative stress and the expression of antioxidants in the liver.

Citations

Citations to this article as recorded by  
  • Cold-shock proteome of myoblasts reveals role of RBM3 in promotion of mitochondrial metabolism and myoblast differentiation
    Paulami Dey, Srujanika Rajalaxmi, Pushpita Saha, Purvi Singh Thakur, Maroof Athar Hashmi, Heera Lal, Nistha Saini, Nirpendra Singh, Arvind Ramanathan
    Communications Biology.2024;[Epub]     CrossRef
  • Early goal-directed management after out-of-hospital cardiac arrest: lessons from a certified cardiac arrest centre
    Birgit Markus, Nikolaos Patsalis, Charlotte Müller, Georgios Chatzis, Leona Möller, Rosita Rupa, Simon Viniol, Susanne Betz, Bernhard Schieffer, Julian Kreutz
    European Heart Journal - Quality of Care and Clinical Outcomes.2024;[Epub]     CrossRef
  • Mechanisms of low-temperature rehabilitation technologies. Natural and artificial hypothermia
    Oleg A. Shevelev, Marina V. Petrova, Elias M. Mengistu, Vladislav A. Yakimenko, Darina N. Menzhurenkova, Irina N. Kolbaskina, Maria A. Zhdanova, Nadezhda A. Khodorovich, Ekaterina O. Sheveleva
    Physical and rehabilitation medicine, medical rehabilitation.2023; 5(2): 141.     CrossRef
  • Continuously increased generation of ROS in human plasma after cardiac arrest as determined by Amplex Red oxidation
    Muhammad Shoaib, Nancy Kim, Rishabh C. Choudhary, Blanca Espin, Mitsuaki Nishikimi, Ann Iverson, Tsukasa Yagi, Seyedeh Shadafarin Marashi Shoshtari, Koichiro Shinozaki, Lance B. Becker, Junhwan Kim
    Free Radical Research.2023; 57(5): 384.     CrossRef
  • Prevention and correction of postdecompression liver dysfunction in obstructive jaundice in experimental animals
    M. M. Magomedov, M. A. Khamidov, H. M. Magomedov, K. I. Hajiyev
    Bulletin of the Medical Institute "REAVIZ" (REHABILITATION, DOCTOR AND HEALTH).2021; 11(4): 45.     CrossRef
  • Hypothermic treatment reduces matrix metalloproteinase-9 expression and damage in the liver following asphyxial cardiac arrest in rats
    Donghwi Kim, Bora Kim, Hyejin Sim, Tae-Kyeong Lee, Hyun-Jin Tae, Jae-Chul Lee, Joon Ha Park, Jun Hwi Cho, Moo-Ho Won, Yoonsoo Park, Ji Hyeon Ahn
    Laboratory Animal Research.2021;[Epub]     CrossRef
  • High Oxygen Does Not Increase Reperfusion Injury Assessed with Lipid Peroxidation Biomarkers after Cardiac Arrest: A Post Hoc Analysis of the COMACARE Trial
    Jaana Humaloja, Maximo Vento, Julia Kuligowski, Sture Andersson, José David Piñeiro-Ramos, Ángel Sánchez-Illana, Erik Litonius, Pekka Jakkula, Johanna Hästbacka, Stepani Bendel, Marjaana Tiainen, Matti Reinikainen, Markus B. Skrifvars
    Journal of Clinical Medicine.2021; 10(18): 4226.     CrossRef
Blood Gases during Cardiopulmonary Resuscitation in Predicting Arrest Cause between Primary Cardiac Arrest and Asphyxial Arrest
Sei Jong Bae, Byung Kook Lee, Ki Tae Kim, Kyung Woon Jeung, Hyoung Youn Lee, Yong Hun Jung, Geo Sung Lee, Sun Pyo Kim, Seung Joon Lee
Korean J Crit Care Med. 2013;28(1):33-40.
DOI: https://doi.org/10.4266/kjccm.2013.28.1.33
  • 2,461 View
  • 22 Download
AbstractAbstract PDF
BACKGROUND
If acid-base status and electrolytes on blood gases during cardiopulmonary resuscitation (CPR) differ between the arrest causes, this difference may aid in differentiating the arrest cause. We sought to assess the ability of blood gases during CPR to predict the arrest cause between primary cardiac arrest and asphyxial arrest.
METHODS
A retrospective study was conducted on adult out-of-hospital cardiac arrest patients for whom blood gas analysis was performed during CPR on emergency department arrival. Patients were divided into two groups according to the arrest cause: a primary cardiac arrest group and an asphyxial arrest group. Acid-base status and electrolytes during CPR were compared between the two groups.
RESULTS
Presumed arterial samples showed higher potassium in the asphyxial arrest group (p < 0.001). On the other hand, presumed venous samples showed higher potassium (p = 0.001) and PCO2 (p < 0.001) and lower pH (p = 0.008) and oxygen saturation (p = 0.01) in the asphyxial arrest group. Multiple logistic regression analyses revealed that arterial potassium (OR 5.207, 95% CI 1.430-18.964, p = 0.012) and venous PCO2 (OR 1.049, 95% CI 1.021-1.078, p < 0.001) were independent predictors of asphyxial arrest. Receiver operating characteristic curve analyses indicated an optimal cut-off value for arterial potassium of 6.1 mEq/L (sensitivity 100% and specificity 86.4%) and for venous PCO2 of 70.9 mmHg (sensitivity 84.6% and specificity 65.9%).
CONCLUSIONS
The present study indicates that blood gases during CPR can be used to predict the arrest cause. These findings should be confirmed through further studies.

ACC : Acute and Critical Care