Preliminary Research Of Neuroprotective Effects Of Moderate Hypothermia & Ketamine On Asphyxiant Cerebral Anoxia In Rats

Objective The aim of this study was to reproduce an asphyxiant cerebral anoxia model with Wistar rats and to investigate the neuroprotective effects of moderate hypothermia and ketamine during a simulative procedure of circulatory collapse in clinical anesthesia. Methods To reproduce a model of asphyxiant cerebral anoxia with Wistar rats, 50 rats were randomly assigned to one of five treatment groups. Group A was sham operation group without apnea. Group B was resuscitated after apnea without any other treatment. Group C was pretreated with ketamine before resuscitation. Group D was pretreated with moderate hypothermia before resuscitation. Group E was pretreated with combined ketamine and moderate hypothermia before resuscitation. The water content of brain, the concentrations of glutamic acid and malondiadehyde (MDA) in brain tissue and the percentage of apoptosis in hippocampus neuron were observed. Results The water content in brain of group B was higher than other groups significantly (P<0.01) except group C (P>0.05). The concentrations of glutamic acid in group B were higher than that of in other four groups significantly (P<0.01). The concentrations of glutamic acid in group E was the lowest among group C, D and E (P<0.01) and the concentration of glutamic acid in group C was a little bit higher than that of in group D (P<0.01). There is no significant difference between group A and group E (P>0.05). The concentrations of MDA in group B were also significantly higher than that of in other four groups (P<0.01). The concentrations of MDA were lower in group C, D and E than that of in group B but higher than that of in group A(P<0.01). Compared to group C, the concentrations of MDA in group D and group E were lower significantly (P<0.01) and there was no difference between the two latter groups (P>0.05). The percentage of apoptosis in hippocampus neurons in group B was higher than that of in other four groups (P<0.01). Compared by effective probability between every two groups, there were no differences in group A, E and C, D (p>0.05). The percentage of apoptosis in hippocampus neurons in group C and group D were higher than that of in group E (P<0.05). Conclusions The model of asphyxiant cerebral anoxia is a better way to simulate the condition of resuscitation after apnea during clinical anesthesia. We can also get much benefits from it to estimate the effects of resuscitation and neural protection. Ketamine can effectively inhibit the release of endogenous glumatic acid and MDA which is the final...