BACKGROUND: The purpose of the present study was to examine the influence of cooling and rewarming conditions using an accurate brain temperature control system. METHOD: 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. FINDINGS: 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). INTERPRETATION: 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.
BACKGROUND: The purpose of the present study was to examine the influence of cooling and rewarming conditions using an accurate brain temperature control system. METHOD: 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. FINDINGS: 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). INTERPRETATION: 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.
Authors: Lina F Chalak; Pablo J Sánchez; Beverley Adams-Huet; Abbot R Laptook; Roy J Heyne; Charles R Rosenfeld Journal: J Pediatr Date: 2013-12-12 Impact factor: 4.406
Authors: Rosemary D Higgins; Tonse Raju; A David Edwards; Denis V Azzopardi; Carl L Bose; Reese H Clark; Donna M Ferriero; Ronnie Guillet; Alistair J Gunn; Henrik Hagberg; Deborah Hirtz; Terrie E Inder; Susan E Jacobs; Dorothea Jenkins; Sandra Juul; Abbot R Laptook; Jerold F Lucey; Mervyn Maze; Charles Palmer; Luann Papile; Robert H Pfister; Nicola J Robertson; Mary Rutherford; Seetha Shankaran; Faye S Silverstein; Roger F Soll; Marianne Thoresen; William F Walsh Journal: J Pediatr Date: 2011-08-27 Impact factor: 4.406
Authors: Joanne O Davidson; Guido Wassink; Lotte G van den Heuij; Laura Bennet; Alistair J Gunn Journal: Front Neurol Date: 2015-09-14 Impact factor: 4.003