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Oxidative Medicine and Cellular Longevity
Volume 2017 (2017), Article ID 8704352, 10 pages
Research Article

Therapeutic Hypothermia Reduces Oxidative Damage and Alters Antioxidant Defenses after Cardiac Arrest

1Departamento de Biofísica, UFRGS, Porto Alegre, Brazil
2Programa de Pós-Graduação em Biologia Celular e Molecular, UFRGS, Porto Alegre, Brazil
3Grupo Hospitalar Conceição, Porto Alegre, Brazil
4Instituto de Ciências Básicas da Saúde, UFRGS, Porto Alegre, Brazil
5Hospital de Clínicas de Porto Alegre, Porto Alegre, Brazil

Correspondence should be addressed to Mara S. Benfato

Received 22 December 2016; Revised 7 February 2017; Accepted 21 February 2017; Published 2 May 2017

Academic Editor: Silvana Hrelia

Copyright © 2017 Fernanda S. Hackenhaar et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


After cardiac arrest, organ damage consequent to ischemia-reperfusion has been attributed to oxidative stress. Mild therapeutic hypothermia has been applied to reduce this damage, and it may reduce oxidative damage as well. This study aimed to compare oxidative damage and antioxidant defenses in patients treated with controlled normothermia versus mild therapeutic hypothermia during postcardiac arrest syndrome. The sample consisted of 31 patients under controlled normothermia (36°C) and 11 patients treated with 24 h mild therapeutic hypothermia (33°C), victims of in- or out-of-hospital cardiac arrest. Parameters were assessed at 6, 12, 36, and 72 h after cardiac arrest in the central venous blood samples. Hypothermic and normothermic patients had similar S100B levels, a biomarker of brain injury. Xanthine oxidase activity is similar between hypothermic and normothermic patients; however, it decreases posthypothermia treatment. Xanthine oxidase activity is positively correlated with lactate and S100B and inversely correlated with pH, calcium, and sodium levels. Hypothermia reduces malondialdehyde and protein carbonyl levels, markers of oxidative damage. Concomitantly, hypothermia increases the activity of erythrocyte antioxidant enzymes superoxide dismutase, glutathione peroxidase, and glutathione S-transferase while decreasing the activity of serum paraoxonase-1. These findings suggest that mild therapeutic hypothermia reduces oxidative damage and alters antioxidant defenses in postcardiac arrest patients.