Although hypothermia as a means of neuronal protection and resuscitation after ischemic damage has a history of approximately four decades, extensive studies on the mechanisms, effects and methods of mild hypothermia at no less than 32°C have been started only in the last decade, both in basic and clinical fields. In experiments on rodents, postischemically introduced hypothermia, even as late as several hours after reperfusion, which was maintained for one day followed by a slow rewarming, definitely rescued hippocampal neurons against damage. Hypothermia appears to have a much greater potential for cerebral resuscitation than any chemical proposed so far for this purpose. The mode of action of hypothermia is apparently nonspecific and multifocal in widely progressing cascade reactions in ischemic cells, including (i) suppressing glutamate surge followed by (ii) intraneuronal calcium mobilization, (iii) postischemic sustained activation of glutamate receptors, (iv) dysfunction of blood-brain barrier, (v) proliferation of microglial cells, and (vi) production of superoxide unions and nitric oxide in microglial cells, and of activator protein-1 in ischemically vulnerable regions like hippocampal CA1. Recent clinical trials of mild hypothermia have revealed significantly beneficial outcomes along with an accumulation of knowhows on various techniques and treatments. Large scale randomized studies involving multiple institutions as well as exchanging ideas are needed for further development of hypothermia treatment.
Biomedical Reviews 1997; 8: 23-36.
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