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.