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目的:创伤导致的失血性休克是临床上常见的导致死亡的原因之一,传统的快速扩容措施会导致缺血-再灌注损伤,诱发炎症反应和组织细胞的凋亡坏死;新型气体信号分子硫化氢(H2S)具有抗炎、促进心血管增生等多种生理保护功能,在此实验中我们探索了新型气体信号分子硫化氢(H2S)对出血性休克大鼠心肌的保护作用。方法:复制雄性SD大鼠出血性休克模型:复制大鼠腹中正切口造成创伤模型,然后经右侧股动脉插管放血,造成失血性休克,右侧股静脉建立液体通道准备复苏,给药组大鼠经腹腔给予NaHS(28μmol/kg),经左侧股动脉插管至左心室监测大鼠血流动力学的影响;取大鼠复苏后2 h静脉血,测量血清肌酸激酶(CK)及乳酸脱氢酶(LDH)水平,比较各组心肌酶改变。以蛋白印记法观察大鼠心肌组织凋亡相关因子Bcl-2、Bax、与Caspase-8的表达变化。结果:外源性H2S对创伤性休克大鼠的血流动力学指标有不同程度的改善,保护了创伤休克导致的心肌细胞的损伤,并上调了大鼠心肌组织中抗凋亡蛋白Bcl-2的表达,下调了促凋亡蛋白Bax及Caspase-8的表达。结论:外源性硫化氢可能通过抑制凋亡途径来保护创伤性休克导致大鼠的心肌组织的损伤,从而起到保护作用。
OBJECTIVE: Traumatic hemorrhagic shock is one of the common causes of death in clinical practice. The traditional rapid expansion measures can lead to ischemia-reperfusion injury, induce inflammatory reaction and apoptosis necrosis of tissue cells. A new type of gas signaling molecule Hydrogen (H2S) has many physiological protective functions such as anti-inflammation and promoting cardiovascular proliferation. In this experiment, we explored the protective effect of a new type of gas signaling molecule hydrogen sulfide (H2S) on the myocardium of hemorrhagic shock rats. METHODS: Hemorrhagic shock model of male SD rats was duplicated: a wound model was created by duplicating the positive incision in the abdomen of the rats and then exsanguinated through the right femoral artery to cause hemorrhagic shock. The right femoral vein was established to establish a fluid channel for resuscitation. The rats were intraperitoneally administered with NaHS (28μmol / kg), the left femoral artery was cannulated to monitor the hemodynamics in the left ventricle. Serum creatine kinase (CK) And lactate dehydrogenase (LDH) levels were compared between the changes of myocardial enzymes. The changes of apoptosis related factors Bcl-2, Bax and Caspase-8 in myocardium were observed by Western blotting. Results: Exogenous H2S improved the hemodynamic parameters of traumatic shock rats to some extent, protected the injury of myocardial cells induced by traumatic shock and up-regulated the expression of anti-apoptotic protein Bcl-2 , Downregulated the expression of pro-apoptotic proteins Bax and Caspase-8. Conclusion: Exogenous hydrogen sulfide may protect the myocardial tissue of rats from traumatic shock by inhibiting the apoptosis pathway.