Objective To investigate the effect of graded hypothermia on neuropathologic alterations of neonatal rat brain after exposed to hypoxic-ischemic insult at 37°C,33°C,31°C,and 28°C,respectively,and to observe the effect of hypothermia on 72-kDa heat shock protein (HSP72) expression after hypoxic-ischemic insult.Methods Seven days old Wistar rats were subjected to unilateral common carotid artery ligation followed by exposure to hypoxia in 8% oxygen for 2 hours at 37°C,33°C,31°C,and 28°C,respectively.The brain temperature was monitored indirectly by inserting a mini-thermocouple probe into the temporal muscle during hypoxia.After hypoxia-ischemia their mortality was assessed.Neuronal damage was assessed with HE staining 72 hours after hypoxia.HSP72 expression at 0.5,24,and 72 hours of recovery was immunohistochemically assessed using a monoclonal antibody to HSP72.Results Hypoxia-ischemia caused 10.5% (2/19) of mortality in rat of 37°C group,but no death occurred in 33°C,31°C or 28°C groups.HE staining showed neuropathologic damage was extensive in rats exposed to hypoxia-ischemia at 37°C (more than 80.0%).The incidence of severe brain damage was significantly decreased in 33°C (53.3%) and 31°C groups (44.4%),and no histologic injury was seen in the 28°C group of rats.Expression of HSP72 was manifest and persistent in the rat brain of 37°C group,but minimum in the rat brain of 28°C group.Conclusion Mild and moderate hypothermia might prevent cerebral visible neuropathologic damage associated with hypoxic-ischemic injury by decreasing stress response. Objective To investigate the effect of graded hypothermia on neuropathologic alterations of neonatal rat brain after exposed to hypoxic-ischemic insult at 37 ° C, 33 ° C, 31 ° C, and 28 ° C, respectively, and observe the effect of hypothermia on Seven-week old Wistar rats were subjected to unilateral common carotid artery ligation followed by exposure to hypoxia in 8% oxygen for 2 hours at 37 ° C, 33 ° C , 31 ° C, and 28 ° C, respectively. Brain temperature was monitored indirectly by inserting a mini-thermocouple probe into the temporal muscle during hypoxia. After hypoxia-ischemia their metric was assessed. Neuronal damage was assessed with HE staining 72 hours after hypoxia.HSP72 expression at 0.5, 24, and 72 hours of recovery was immunohistochemically assessed using a monoclonal antibody to HSP72. Results Hypoxia-ischemia caused 10.5% (2/19) of mortality in rat at 37 ° C group, but no death occurred in 33 ° C, 31 ° C o The incidence of severe brain damage was significantly decreased at 33 ° C (53.3%) and at 31 ° C (more than 80.0%) at 28 ° C in the groups exposed to hypoxia-ischemia ° C groups (44.4%), and no histologic injury was seen in the 28 ° C group of rats. Expression of HSP72 was manifest and persistent in the rat brain of 37 ° C group, but minimum in the rat brain of 28 ° C group.Conclusion Mild and moderate hypothermia might prevent cerebral visible neuropathologic damage associated with hypoxic-ischemic injury by decreasing stress response.