失血性休克大鼠血浆S100B蛋白的动态测定

目的探讨失血性休克大鼠血浆S100B蛋白动态变化及其临床价值。方法选择无特定病原体级成年大鼠10只，通过急性失血损伤方式建立收缩压下降曲线，形成失血性休克动物模型，测定大鼠收缩压基础值（T1），记录收缩压降至基础值3／4（T2）、基础值2，3（T3）、基础值1／2（T4）、基础值2，5（T5）、30mmHg（T6）、基础值1／5（B）、10mmHg（T8）失血量，采用酶联免疫吸附分析检测各个时间点血浆S100B蛋白含量。结果T2和B、T5和T6、T7和T8间失血量有统计学意义（P〈0．05），而其它相邻时间点之间无显著差异（P〉0．05）；T3和T4、T4和T5之间血浆S100B蛋白含量差异显著（P〈0．05），而其它相邻时间点之间无显著差异（P〉0．05）；不同时间点失血量和S100B蛋白含量无显著相关性（P〉0．05）。结论建立收缩压下降曲线的失血性休克大鼠模型，可评估失血量变化，结合S100B蛋白水平动态监测，可对脑组织细胞损伤发展程度进行有效评估。

Dynamic observation of plasma level of S-100B protein in rats with traumatic bleeding shock

Objective To explore the dynamic changes in the plasma levels of S-100B protein in rats with traumatic bleeding shock. Methods The model of the traumatic bleeding shock （THS） with gradient decrease in the systolic blood pressure was established in 10 rats without specific pathogen. The arterial blood during the different phase of shock, i.e. when the systolic pressures were three forth, two third, one second, two fifth of the basis systolic blood pressure, 30 mmHg, one fifth of the basic systolic blood pressure and 10 mmHg, was collected and S-100B protein levels in the plasma were determined by the double antibody sandwich method of enzyme-labeled immunosorbent assay （ELISA） and analyzed. Results There were significant differences in plasma levels of S-100B protein between the rats with two third of the basic systolic blood pressure and the rats with one second of the basic systolic blood pressure, and the rats with two fifth of the basic systolic blood pressure and the rats with 30mmHg systolic blood pressure （P〈0.05）. Conclusions The plasma level of S-100B protein is related to the systolic pressure during the shock. The present study suggestes that the decrease in the systolic pressure to one second of the basic systolic pressure, or to 10 mmHg may produce significant increase in the plasma level of S-IOOB protein. The dynamic observation of the plasma level of S-100B protein which is a good index of the damage to the cerebral cells, may be helpful to assessment of the degree of damage to the cerebral cells.