Do rapid systemic changes of brain temperature have an influence on the brain?

The purpose of the present study was to examine the influence of cooling and rewarming conditions using an accurate brain temperature control system.

The brain temperature of animals was measured with a thermometer while feedback regulation was achieved with a cold (4( degrees )C) and hot (50( degrees )C) water on-off flow system. Brain temperature was well controlled throughout the experiment by using both cold water and hot water simultaneously. Three groups were studied, as follows: 1) the standard group (cooled to 24( degrees )C for 1 hour, kept at 24( degrees )C for 2 hours and rewarmed to 37( degrees )C for 1 hour), 2) the rapid-cooling group (cooled to 24( degrees )C for 30 min, kept at 24( degrees )C for 2 h, and rewarmed to 37( degrees )C for 1 h), 3) the rapid-rewarming group (cooled to 24( degrees )C for 1 h, kept at 24( degrees )C for 2 h, and rewarmed to 37( degrees )C for 30 min) and the normal-control group.

An increase of MAP-2 immunoreactivity of the CA1 neurons in the dorsal hippocampus was observed one week but not one month after hypothermia in the rapid-rewarming group. There was also a significant increase in the glutamate and lactate value at the end of rewarming compared with the baseline in the rapid-rewarming group (p<0.01).

Our results suggest that rapid rewarming after hypothermia triggered an uncoupling of cerebral circulation and metabolism, inducing an increase of extracellular glutamate and lactate, consequently reversible neuronal cell damage.