• Kenji Dohi, Kazuyuki Miyamoto, Kenichiro Fukuda, Shunsuke Nakamura, Munetaka Hayashi, Hirokazu Ohtaki, Seiji Shioda, and Tohru Aruga.
• Department of Emergency and Critical Care Medicine, Showa University Fujigaoka Hospital, Aoba-ku, Yokohama, Kanagawa 227-8501, Japan. kdoppy@yahoo.co.jp
• Oxid Med Cell Longev. 2013 Jan 1;2013:562429.

AbstractTherapeutic hypothermia (TH) is thought to be due to the downregulation of free radical production, although the details of this process remain unclear. Here, we investigate changes in oxidative stress and endogenous biological antioxidant potential during TH in patients with post-cardiac arrest syndrome (PCAS). Nineteen PCAS patients were enrolled in the study. Brain temperature was decreased to the target temperature of 33°C, and it was maintained for 24 h. Patients were rewarmed slowly (0.1°C/h, <1°C/day). The generation of reactive oxygen metabolites (ROMs) was evaluated in plasma samples by d-ROM test. Plasma antioxidant capacity was measured by the biological antioxidant potential (BAP) test. Levels of d-ROMs and BAP levels during the hypothermic stage (33°C) were suppressed significantly compared with pre-TH induction levels (P < 0.05), while both d-ROM and BAP levels increased with rewarming (33-36°C) and were correlated with brain temperature. Clinical monitoring of oxidative stress and antioxidant potential is useful for evaluating the redox state of patients undergoing TH after PCAS. Additional therapy to support the antioxidant potential in the rewarming stage following TH may reduce some of the observed side effects associated with the use of TH.

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