乌司他丁对创伤失血性休克兔细胞因子和黏附分子的影响

Effects of ulinastatin on cytokines and intercellular adhesion molecule in traumatic hemorrhagic shock in rabbits

目的通过测定创伤失血性休克兔血清细胞因子(TNF-α、IL-8)和可溶性细胞间黏附分子-1(sICAM-1),以及肺组织病理学改变,评价乌司他丁对创伤失血性休克的疗效及对缺血再灌注损伤的保护作用。方法将新西兰白兔30只随机分为3组:对照组、创伤失血性休克生理盐水组和创伤失血性休克乌司他丁组。分别在休克前、休克末、复苏后2h、4h各时相点静脉采血测定细胞因子(TNF-α、IL-8)及可溶性细胞间黏附分子-1(sICAM-1)。复苏后4h空气栓塞处死动物,取右下肺叶组织观察病理变化。结果对照组TNF-α、IL-8在各时点变化不明显。另外2组在TNF-α水平变化明显升高,且生理盐水组高于乌司他丁组(P<0.05)。而生理盐水组IL-8在复苏后4h才较对照组明显增高(P<0.05),而且辐度大于乌司他丁组(P<0.05)。肺组织病理学观察显示乌司他丁对缺血再灌注损伤肺具有保护作用。结论乌司他丁可能通过抑制TNF-α、IL-8和sICAM-1的释放,对创伤失血性休克及其引起的缺血再灌注肺损伤产生保护作用。

Objective To investigate the influences of ulinastatin on serum levels of cytokines and intercellular adhesion molecule and to evaluate the protective effects of ulinastatin on pulmonary function in traumatic hemorrhagic shock in rabbits. Methods Thirty rabbits were randomly divided into three groups: control group, traumatic hemorrhagic shock group and ulinastatin-treated group. Blood samples were collected at the four time points: pre-shock, post-shock, as well as 2h and 4h after blood volume compensation. Serum levels of TNF-α, IL-8 and sICAM-1 were determined. 4h after blood volume compensation, the rabbits were killed, and the lung samples were taken for histological analysis. Results In control group, the serum concentrations of TNF-α, IL-8 and sICAM-1 showed no obvious changes during the experiment. However, in shock group and ulinastatin-treated group the serum concentrations of TNF-α, IL-8 and sICAM-1 increased significantly in the duration of experiment compared with the pre-shock levels(P<0.05), moreover, the serum concentrations of above indexes in ulinastatin-treated group were significantly lower than those in shock group at corresponding time points(P<0.05). The changes of histological structure showed the protective effects of ulinastatin on ischemia/reperfusion injury in the rabbit lung in traumatic hemorrhagic shock. Conclusion Ulinastatin possesses some protective effects to the lung tissue in traumatic hemorrhagic shock, which may be attributed to the decrease of the release of TNF-α, IL-8 and sICAM-1.