Small reductions in temperature during anoxia-induced white matter injury can strongly and favorably influence nerve functional outcome. Using the in vitro optic nerve anoxia model to evaluate the effect of temperature (through a 10°C range, 32-42°C) on postanoxic CAP, Stys et al. (1992b) observed that there were protective effects of lower temperature and worsened outcomes from increased temperature. Lowering temperature by only 2.5°C during anoxic exposure resulted in near doubling of CAP recovery during the postanoxic period (65% recovery at 34.5°C vs. 35% at 37°C). Reducing temperature further, by a total of 5°C (37-32°C), resulted in complete recovery of post-anoxic CAP. The converse relationship, of worsened functional recovery at higher temperature, was also seen.

The neuroprotective mechanism of action of hypothermia is not entirely clear. It may be due to reduced metabolic requirements of hypothermic tissue including white matter, since it is known that oxygen consumption is reduced on the order of 6% to 8% per degree C from 37°C (Nishizaki et al., 1988), which extrapolates to a 15% to 20% total reduction of oxygen consumption for a 2.5°C drop. However the Q10s of other events in the axonal injury cascade may also contribute to the protective effect of hypothermia. As discussed above, the reversal of the Na+/Ca2+ exchanger is a critical step in the final influx on calcium into axons, and it is known that the rate of Ca2+ movement through this exchanger is highly temperature-dependent, with lower temperatures causing slower exchange (Russell and Blaustein, 1974).

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