Effects Of Hypothermia On Glucose Following Severe Craniocerebral Trauma In Rats

Background and purpose: Hypothermia therapy was used inmedicine several centuries ago and was tried in brain diseasesin the early of 19th century. There was not a satisfying resultdue to shortcoming of the study methods and there were frequentlysevere complications, such as, shivering, arrhythmia,coagulation disorders and increased risk of infection(pulmonary infection), and so on. As a result, the applicationof hypothermia in medicine was limited. For the first time, Jiangindicated that the temperature of 30~34癈 had significantlybrain protection to the animals with craniocerebral trauma in1991, then the study about hypothermia has renewed interest.Most prospective clinical studies suggest hypothermia therapycan significantly improve the outcome following severecraniocerebral trauma. But the mechanisms by which hypothermia is neuroprotective are not fully understood yet. The aim of the article is to study the effect of hypothermia on glucose following severe craniocerebral trauma in rats, providing one of the mechanisms of protective effects of hypothermia.Methods: Brain trauma was induced on left cerebrum by freefalling objects. 25 male SD rats were divided randomly into threegroups: the control group(non-traumatic animals, n=5),thenormothermia group (traumatic animals, n=10) and thehypothermia-treated group(traumatic animals, n=10).The wholebody of the animals in the hypothermia-treated group was cooledto 33. 0 + 1. 5 for 150 minutes, then the animals were rewarmed38. 0 + 0. 5℃ naturally. The whole body of the animals in thenormothermia group was controlled about 38. 0 + 0. 5℃. The corebody temperature of the animals was monitored continuously viaa rectal probe. The blood samples were obtained at pre-operationand post-operation of 3, 8, 24 , and 48 hours respectively. Theblood glucose was measured with spectrophotometer by enzymaticmethod. The rats were killed at post-operation of 72 hours andbrain tissue was taken out as fresh as possible. The area oftraumatic brain was inspected by naked-eye and opticalmicroscope.Results: (1) Brain macrostructure: We could see focal cortical necrosis, cavitation of the cerebral tissue, subarachnoid hemorrhage, subdural hematomas and epidural hematoma. (2) Histopathological examination: Hemorrhagic changes and ischemic changes could be seen at the cerebral cortex, basal nuclei, upper brainstem. (3) No significant differences were noted in false operational groups. The values of blood glucose were 8. 02?. 71, 7. 97 + 0. 86 and 8. 11?. 97mmol/L during 3, 8, 24 hour respectively in the normothermia group(P<0.05). But the values of blood glucose were 5. 90 + 0. 67, 6. 18 + 0. 66 and 6. 19 + 0.61mmol/L during 3, 8, 24 hour respectively in the hypothermia-treated group(P>0.05). However, there was significant difference between normothermia and hypothermia group (P<0. 05).Conclusion: These data suggest hypothermia therapy can reduce the level of blood glucose following craniocerebral trauma. As a result, it can ameliorate secondary brain damage about the disturbance of glycometablism following craniocerebral trauma and improve neurological function. These results suggest that a contributing factor to the cerebroprotective effects of hypothermia in craniocerebral trauma may be related to the reduction of the levels of bloodglucose following trauma.