亚低温对重型颅脑损伤后葡萄糖代谢影响的实验研究

The effects of hypothermia on blood glucose after severe craniocerebral trauma in the rats

目的研究亚低温治疗对重型颅脑损伤大鼠血糖的影响。方法25只雄性SD大鼠随机分为三组:假手术组、常温组和亚低温治疗组。采用硬膜外自由落体打击法制作颅脑损伤模型。监测直肠温度,亚低温治疗组保持大鼠体温在33.0±1.5℃。常温组维持大鼠通常体温(为38.0±0.5 ℃)。分别于术前、术后3、8、24和48 h取血,检测血糖含量,测定其基础值及伤后动态变化。结果实验性颅脑损伤后血糖明显升高,于伤后24 h达到最高水平。常温组伤后各时段血糖值与基础值比较有显著差异(P<0.05)。亚低温治疗组伤后各时段血糖值与基础值比较无显著差异(P>0.05),但其伤后各时段血糖值与常温组各时段血糖值比较有显著差异(P<0.05),表明亚低温治疗可抑制重型颅脑损伤后高血糖反应。结论亚低温治疗可抑制颅脑损伤后高血糖反应,这有利于减轻颅脑损伤后糖代谢障碍所致脑组织的继发性损害。抑制颅脑损伤后高血糖反应可能是亚低温脑保护机制之一。

Objective To study the effect of hypothermia on blood glucose levels after severe craniocerebral trauma in rats, and understand one of the protective mechanisms of hypothermia. Methods25 male SD rats were divided randomly into 3 groups: the pseudo operation group (non-trauma animals, n=5), the normothermia group (traumatic animals, n=10) and the hypothermia-treated group(traumatic animals, n=10). Brain trauma was induced by free falling objects. The temperature of the animals in the hypothermia-treated group was cooled to 33.0±1.5 ℃, it was kept at 38.0 ±0.5 ℃in the normothermia group. The temperature of the animals was monitored continuously via a rectal probe. The blood samples were obtained at pre-operation and post-operation (trauma) of 3, 8, 24 and 48 hours respectively. The blood glucose was examined with spectrophotometer by enzymatic method. Results No significant differences of blood glucose were noted in pseudo operation group(5.84±0.23 ~ 6.55±0.33 mmol/L). The values of blood glucose was 8.02±0.71, 7.97±0.86 and 8.11±0.97 mmol/L during 3, 8, 24 hours post-trauma respectively in the normothermia group, which has significant difference compared with pseudo operation group (P<0.05). But the values of blood glucose was 5.90±0.67, 6.18±0.66 and 6.19±0.61 mmol/L during 3, 8, 24 hours respectively in the hypothermia-treated group, which showed no significant difference compared with pseudo operation group (P>0.05). However, there was significant difference between normothermia and hypothermia group of blood glucose (P<0.05). Conclusion These data demonstrated that hypothermia inhibit the rising of blood glucose level after craniocerebral trauma. It may be induced that hypothermia attenuates secondary brain damage caused by the disturbance of glycometablism and thus improve neurological function. The inhibition of blood glucose level may be an important factor in the neuroprotective effect of hypothermia.