Hypothermia Treatment Of Traumatic Brain Injury, Experimental Studies

Objective:To set up severe head injury treated with mild hypothermia model. Methods:120 SD rat randomly divided into 8 groups (n=15 in each group): before cooling , cooling 6/12/24/48/72/96/120h. The model was induced by dropping a weight of 60g from a height of 50cm onto the epidura and treating with mild hypothermia(32~34℃ ). Blood pressure and ECG were observed. Serum K+,Na+,Mg2+ levels were measured. The change of neuron microstructure in rat cerebral traumatic tissue of every group was observed by transmission electron microscope. Results:Animal mortality increased and serum K+,Mg2+ levels gradually decreased with the treating time was increased. Serum Na+ has not signally change. There is one rat in 72h group ,two rats in 96h and two rats 120h group with bradytachycardia.The results observed by transmission electron microscope showed that the rat's encephaledema present gradual relieving trend during mild hypothermia treatment.There is one rat in 96h group and one rat in 120h group with diffuse tubuli renales necrosis. Pathological and pathophysiological changes was emerged. Conclusion : The established model was in conformity with the characteristics of vital sign,serum electrolyte and cerebral microstructure of severe head injury patients treated with mild hypothermia clinically.Objective: Evaluating the effects of mild hypothermia on the rat cerebral morphologic changes in different times when severe head injury and the suitable treating. times Methods:(1)Set up severe head injury treated with mild hypothermia model. The rats randomly divided into 15 groups (n=15 in each group): normal group , trauma 6/12/24/48/72/96/120h group , cooling 6/12/24/48/72/96/120h group. (2) Observing the cerebral pathologic changes of the rat when severe head injury after H-E staining through light microscope. Observing the changes of mitochondria by using transmission electron microscope. Measuring the expression of nNOS mRNA through RT-PCR. Measuring the activity of iNOS. Results:(1) Mitochondria Rsv present uptrend after injuring 6-12h.Itpresent droptrend from injuring 72h. Mitochondria Rsv in cooling 6/12/24/48/72h are significant smaller than those in corresponding trauma groups (p<0.05) . There is no different between mitochondria Rsv in cooling 96/120h and corresponding trauma groups (p>0.05). (2) The OD of nNOS in trauma and cooling 6/12/24/48/72/96h group are obviously higher than that in normal group (p<0.05) . There is no different between the OD of nNOS in normal, trauma and cooling 120h group(p>0.05). The OD of nNOS present uptrend in trauma and cooling 6/12/24h group. They in cooling 6/12/24 group are obviously lower than those in corresponding trauma groups(p<0.05) . It present droptrend from injuring 48h. There is no different between the OD of nNOS in trauma and cooling 48/72/96/120h group(p>0.05). (3) The activity of iNOS in trauma and cooling 12/24/48/72/96/120h group are obviously higher than that in normal group (p<0.05) . There is no different between the activity of iNOS in normal, trauma and cooling 6h group(p>0.05). The activity of iNOS present uptrend in trauma and cooling 12/24/48/72h group. They in cooling 12/24/48/72h group are obviously lower than those in corresponding trauma groups(p<0.05) . The activity of iNOS stood in flat stage in trauma and cooling 96/120h group. There is no different between the activity of iNOS in trauma and cooling 96/120h group(p>0.05). Conclusion:(1) nNOS mediates rat cerebral ischemia and the changes of mitochondria structure during early head injury. In reperfusion stage, nNOS'neurotoxic is not the most important in rat head injury. There is other mechanisms in rat head injury. (2) iNOS mediates rat cerebralischemia and the changes of mitochondria structure in reperfusion following ischemia when head injury. (3) Hypothermia treatment play a treatable role less than injuring 72h . It did not play a obvious treatable role after injuring 72h. Hypothermia treatment's suitable treating times less than injuring 72h.Objective: Evaluating NOS's generati...