Postischemic moderate hypothermia inhibits CA1 hippocampal ischemic neuronal injury.
We have determined whether lowering brain temperature during the acute recirculation period following transient cerebral ischemia would influence the extent of ischemic neuronal injury. Anesthetized rats underwent 10 min of bilateral carotid artery occlusion combined with systemic hypotension (50 mmHg). Four animal subgroups were investigated, including non-ischemic controls; rats whose postischemic brain temperature was maintained at 36 or 30 degrees C starting 5 min into the recirculation period; and rats in which postischemic hypothermia was begun 30 min into the recirculation period. In all cases, intra-ischemic brain temperature was 36 degrees C and body temperature was held at 36-37 degrees C throughout. Three days following the ischemic insult, the CA1 sector of the hippocampus was severely damaged in normothermic rats (36 degrees C). In contrast, when postischemic brain temperature was decreased to 30 degrees C starting 5 min into the recirculation period, normal-appearing pyramidal neurons were present throughout the CA1 hippocampus. A beneficial effect of postischemic hypothermia was not demonstrated when brain cooling was initiated 30 min into the recirculation period. These results demonstrate that postischemic hypothermia can markedly protect CA1 pyramidal neurons from injury following transient ischemia. The 'therapeutic window' for postischemic hypothermia was found to be narrow under the present experimental conditions.
Busto
R
R
Department of Neurology, University of Miami School of Medicine, FL 33101.
Dietrich
W D
WD
Globus
M Y
MY
Ginsberg
M D
MD
D000818:Animals; D007036:Hypothermia, Induced; D002546:Ischemic Attack, Transient / Q000150:complications / Q000473:pathology / Q000628:therapy*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains