脊髓缺血再灌注损伤中热休克蛋白表达的研究

目的研究脊髓缺血再灌注损伤(SCII)后热休克蛋白(HSP70)表达的变化。方法制作SCII动物模型,采用光镜、激光多普勒超声、免疫组化等技术,研究SCII后HSP70表达的变化。结果(1)缺血30min,血灌流量平均下降85.37%,再灌流即刻血灌流量迅速升高,再灌流10min左右达到最高点。再灌流30min,血灌流量基本恢复到缺血前的基线水平,以后逐渐降低。(2)缺血后部分大鼠再灌注后出现“二次瘫痪”现象。(3)脊髓缺血30min再灌注60min后即有HSP70的表达增强,随着再灌注时间的延长,HSP70表达逐渐增多,在再灌注240min达到高峰。此后,HSP70表达逐渐减少,在再灌注24h基本消失。结论(1)脊髓缺血一定时间后恢复血液供应,可以发生再灌注损伤。(2)脊髓缺血再灌注后HSP70的表达增加。

Roles of HSP70 on spinal cord neurons in spinal cord ischemia and reperfusion injury

Objective To study the expressions of HSP70 after spinal cord ischemia and reperfusion injury (SCII).Method The animal model was prepared.Hemodynamic changes of the lumbar spinal cord were measured through laser doppler flowmetry.Morphologic changes were examined by microscopy.The expression of IEGs was detected through immunohistochemisty method.Result (1)After 30 min of ischemia, the SCBF decreased rapidly to 85.3% of the mean baseline level. It increased immediately at the moment of reperfusion onset and got to the top value after 10 min of reperfusion. The SCBF approximately decreased to the baseline level and kept lower under the baseline after 30min of reperfusion.(2)Some rats became paralysis the second time in group of 30 min of ischemia.(3)After 60 min of reperfusion, the HSP70 expression was detected, and got to top at 240 min after reperfusion. There was almost no positive immunoreactive neuron after 24 h of reperfusion.Conclusion (1)The injury can occur after spinal cord ischemia and reperfusion.(2)There is overexpression of HSP70 after SCII.