Key result
Mild therapeutic hypothermia reduced malondialdehyde and protein carbonyl levels and increased erythrocyte antioxidant enzyme activity compared to controlled normothermia after cardiac arrest.
Why the study?
Does mild therapeutic hypothermia reduce oxidative damage and alter antioxidant defenses in patients with postcardiac arrest syndrome compared to controlled normothermia?
Observational (n=42)
Does mild therapeutic hypothermia reduce oxidative damage and alter antioxidant defenses in patients with postcardiac arrest syndrome compared to controlled normothermia?
Mild therapeutic hypothermia (33°C) for 24 hours reduces oxidative damage markers and alters antioxidant enzyme activity in patients following cardiac arrest, providing mechanistic insight into its protective effects.
May indicate reduced oxidative stress with hypothermia post-arrest; leaves open impact on neurologic outcomes.
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.
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Hackenhaar et al. (2017) conducted an observational in Postcardiac arrest syndrome (n=42). Mild therapeutic hypothermia vs. Controlled normothermia (36°C) was evaluated on Oxidative damage and antioxidant defenses. Mild therapeutic hypothermia reduced malondialdehyde and protein carbonyl levels and increased erythrocyte antioxidant enzyme activity compared to controlled normothermia after cardiac arrest.
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