Potential neuroprotective effects with mild to moderate cerebral cooling have been clearly demonstrated after experimental hypoxic-ischemic injury.¹ However, the difficulties of establishing an effective regime in clinical practice are formidable. In the absence of definitive evidence of clinical efficacy, it is essential that hypothermia be used safely. Pilot studies have suggested that, under tightly defined conditions, hypothermia is generally safe even in the severely asphyxiated infant,^2-4 and multicenter, randomized, controlled trials are currently underway to further investigate different hypothermic strategies. Many of the clinical issues raised by Thoresen and Whitelaw⁵ can be readily understood in relation to the physiology of adaptation to hypothermia, including both the conservation and production of heat.

Hypothermia leads to rapid peripheral vasoconstriction, ie, centralization of blood flow. This vasoconstriction occurs in a spatially and temporally controlled manner, dependent on tightly integrated input from central and skin thermoreceptors.⁶ Although both core and skin temperatures are physiologically relevant, . . . [Full Text of this Article]