The most attractive feature of induced hypothermia as a neuroprotective strategy is that its neuroprotective action appears to operate via multiple mechanisms. Hypothermia has been shown to alter metabolic rate (4) by decreasing cellular metabolism, thus retarding high-energy phosphate depletion and facilitating postischemic glucose utilization (5). Hypothermia attenuates the cytotoxic cascade by suppressing elevations of intracellular calcium, thereby inhibiting the release of excitotoxic amino acids and reducing intracellular acidosis (6-9).
Hypothermia suppresses the breakdown of the blood-brain barrier (10,11) and reduces free radical formation (9,12). Mild-to-moderate hypothermia might even protect the injured neurovascular tissues against the toxic effects of recombinant tissue plasminogen activator (rtPA), while still allowing the lytic effect to function (13). Hypothermia also prevents cell injury from leading to apoptosis (14), which is believed to be mediated by inhibition of caspase activation (14-16).
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