MILD HYPOTHERMIA FAILS TO PROTECT LATE HIPPOCAMPAL NEURONAL LOSS FOLLOWING FOREBRAIN CEREBRAL-ISCHEMIA IN RATS

Anaesthetized male rats (n = 86) from both Long-Evans strain (LES) (n = 43) and Wistar strain (WS) (n = 43) were utilized for the experiment s. While three animals from each strain were used as control, 40 rats from each strain underwent up to 10 minutes forebrain ischaemia by bil ateral common carotid artery (CCA) occlusion combined with systemic hy potension [Mean Arterial Blood Pressure (MABP) = 50 mm/Hg]. The animal s from each strain were divided into four (n = 10) groups. In both str ains, groups (n = 10) 1 and 2, temporalis muscle (TM) and body tempera tures of the animals were kept at 36-37 degrees C during the experimen ts. The groups 1 and 2 were killed in 3 and 7 days after the ischaemic insult, respectively. The groups 3 and 4 were also killed 3 and 7 day s after the ischaemic insult, but the forebrain ischaemia was carried our under mild cerebral hypothermia (TM temperature = 33 degrees C). P yramidal neurons of the hippocampal CA1 region from each group was eva luated semiquantitatively. In WS, groups 1 and 2 showed moderate and s evere neuronal loss in the CA1 region, respectively. However, in LES w hile the group 1 (3 days survival) did not show any neuronal loss, gro up 2 showed moderate neuronal loss of the CA1 region. While in group 3 (3 days survival, hypothermia) WS and LES, hypothermia protected the CAI region, group 4 of LES showed mild neuronal loss. However WS, grou p 4 (7 days survival, hypothermia) showed severe neuronal loss of the CA1 region. It was concluded that mild hypothermia during ischaemic in sults did not prevent the delayed postischaemic neuronal damage of the hippocampal CA1 region of both strains, and following 10 minutes fore brain ischaemia, male LES rats were found more resistant than male WS rats to neuronal loss of the CA1 region.