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

Fernanda S Hackenhaar,Vanessa M Oliveira,Cleber Verona,Tássia M Medeiros,Fernanda M Heemann,Camila D Mahl,Maria C Guerra,Silvia R R Vieira,Carlos A S Gonçalves,Mara S Benfato,Camile S Behling,Jordana S Putti,Ana Carolina A Da Silva,Diego F M Riveiro

doi:10.1155/2017/8704352

Abstract

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.

Highlights

Postcardiac arrest syndrome (PCAS) refers to the pathophysiological consequences of return of spontaneous circulation (ROSC) after successful cardiopulmonary resuscitation (CPR) for cardiac arrest (CA)
The present study aimed to investigate oxidative stress during PCAS by assessing oxidative stress parameters at 6, 12, 36, and 72 h after CA in intensive care unit (ICU) patients and by comparing patients treated with controlled normothermia versus Mild therapeutic hypothermia (MTH)
After rewarming, d-ROM levels returned to control-group levels, different from the results reported in the present study, where MDA and carbonyl levels remained lower in the Venous pH xanthine oxidase (XO)

Summary

Introduction

Postcardiac arrest syndrome (PCAS) refers to the pathophysiological consequences of return of spontaneous circulation (ROSC) after successful cardiopulmonary resuscitation (CPR) for cardiac arrest (CA). PCAS comprises brain injury, hemodynamic dysfunction, damage to the heart and other organs, sepsis, and systemic inflammation consequent to ischemia-reperfusion (I/R) injury. During PCAS, damage to the brain, heart, and other organs resulting from I/R has been attributed to oxidative stress, as the sudden return of oxygen to circulation increases the generation of reactive oxygen species (ROS) [2, 3]. Generation of ROS, especially superoxide radical, increases dramatically after reperfusion and depends on xanthine. Endothelial XOR plays a well-known role in free radical generation during hypoxia and reperfusion, when xanthine dehydrogenase (XDH) is converted to xanthine oxidase (XO), using oxygen as an electron acceptor instead of nicotinamide adenine dinucleotide (NAD+), generating superoxide and hydrogen peroxide [6]

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