高渗氯化钠羟乙基淀粉溶液对未控制出血性休克大鼠炎性反应的影响

目的:探讨高渗氯化钠羟乙基淀粉溶液(HHS)对未控制出血性休克(UHS)大鼠炎性反应的影响。方法:采用修订的Capone等方法制备创伤UHS模型。30只SD大鼠随机分为3组:NC组(正常对照组)、NS组(生理盐水复苏组)、HHS组(高渗氯化钠羟乙基淀粉溶液复苏组)。分别在伤后0、30、90、210min观察3组大鼠的心率;血清K+、Na+、Cl-的浓度;血浆TNF-α、IL-1β、IL-6、IL-10的浓度。结果:大鼠休克后心率显著下降,复苏后明显升高;HHS组在伤后90min时,血清Na+、Cl-浓度明显增加(P<0.05),但在伤后210min时恢复正常;两复苏组中TNF-α在休克后迅速升高,复苏后进一步上升,IL-1β与IL-6浓度在伤后90min才有明显增加,而IL-10浓度在伤后210min降低(P<0.05)。与NS组比较,HHS组在各相应时点的TNF-α、IL-1β、IL-6浓度明显下降,IL-10浓度显著增高(P<0.05)。结论:HHS有利于保持UHS大鼠血流动力学稳定,并减少促炎因子释放,促进抗炎因子合成,从而对机体产生一定的保护作用。

Effects of hypertonic sodium chloride hydroxyethyl starch 40 on inflammatory response to uncontrolled hemorrhagic shock in rats

Objective To investigate the effect of hypertonic sodium chloride hydroxyethyl starch 40(HHS)on inflammatory response to uncontrolled hemorrhagic shock in rat. Methodes A rat model of uncontrolled hemorrhagic shock was established using the modified Capone method. SD rats (n = 30) were randomly divided into 3 groups, including NC group (normal control group), NS group(normal saline group) and HHS group(hypertonic sodium chloride hydroxyethyl starch 40 group). Heart rate(HR), electrolyte and plasma TNF-α、IL-1β、IL-6 and IL-10 level at various stages of shock and reperfusion were determined and recorded. Results The HR in HHS group and NS group was significantly higher after resuscitation than that after shock (P < 0.05). Compared with NS group and NC group, the serum Na+ and Cl- concentration in HHS group increased at 90 min after injury, but restored to normal level at 210 min after injury. Plasma TNF-α、IL-1β and IL-6 level markedly increased after hemorrhagic shock and reperfusion in group NS and group HHS, in addition, plasma TNF-α、IL-1β and IL-6 level were significantly lower in group HHS than those in group NS. Plasma IL-10 level obviously decreased at 210 min after injury in group NS and group HHS, and plasma IL-10 level was significantly higher in group HHS than that in group NS (P < 0.05). Conclusion Hypertonic sodium chloride hydroxyethyl starch 40 contributes to the stabilization of hemodynamics and can protect rat against uncontrolled hemorrhagic shock by inhibiting the release of the proinflammatory factors and improving synthesis of anti-inflammatory factors, and restoring the stationarities among cytokine networks.