抄録
Therapeutic hypothermia is well known to even lay citizens as a treatment for brain injury today. The treatment was initially introduced into clinical practice in the 1930s. However, since performing systemic cooling below 30°C caused various severe complications, i.e. infection, cardiac failure and so on. Because of those, hypothermic treatment did not appear to benefit patients with brain and become obsolete by the end of 1980s. In the early 1990s, mild hypothermia (MH) (32~34°C) therapy was demonstrated to have significant neurological protective effects similar to those of the previous deep hypothermic therapy. Since MH does not require rigorous patient management so much as deep hypothermia during hypothermia therapy, it has been widespread dramatically all over the world.
Hypothermic treatment is thought to prevent secondary brain damage induced by ischemic brain insults by inhibiting calcium loading, excessive glutamate release and free-radical derivation. In clinical brain emergence, an early induction of MH could minimize the brain damage and result in better outcome. Results of many laboratory works have supported the beneficial effect of MH. However, in clinical setting, the efficacy of MH remained unproved.
In 2002, two prospective, randomized studies reported improved outcomes when hypothermia was induced in comatose survivors after resuscitation from cardiac arrest. MH was shown to mitigate brain damage significantly when induced before, during, and after cardiac arrest. In today talk, I will review therapeutic hypothermia with an emphasis on mild resuscitative hypothermia. [Jpn J Physiol 54 Suppl:S56 (2004)]
