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目的：研究中药提取物丹参酮IIA 磺酸钠在创伤失血性休克中的作用。方法：复制SD 大鼠创伤失血性休克模型，即经右侧股动脉插管放血，左侧股静脉建立液体通道，经颈动脉插管至左心室监测创伤失血性休克大鼠平均动脉压；在达到最大放血量后，治疗组大鼠给予丹参酮IIA 磺酸（10mg/ kg）。按时间点经股静脉取大鼠静脉血，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。并以酶联免疫法检测各组大鼠血清促炎因子IL-Iβ、IL-6、IL-10 和TNFα的改变。结果：丹参酮IIA 磺酸钠在一定程度上改善了创伤失血性休克导致大鼠的血流动力学的改变，显著减轻了炎症反应过程中的各种炎症因子的表达。结论：丹参酮IIA 磺酸钠改善了创伤失血性休克导致大鼠的低血压；抑制了大鼠创伤失血性休克过程中炎症因子的表达，可能在创伤失血性休克过程中发挥保护作用，为临床提供了疗创伤失血性休克提供了新的可能的参考。

英文摘要:

Objective: To investigate the protective effects of Tanshinone IIA Sodium Sulfonate on the traumatic-hemorrhagic shock. Methods: Duplicate traumatic-hemorrhagic shock models of SD rats; that is, drawing blood from right femoral artery; establishing liquid pathway through left femoral artery; monitoring the mean arterial pressure; detecting the concentrations of creatine kinase (CK) and lactate dehydrogenase (LDH). Inflammatory cytokines concentrations of IL-1B, IL-6, IL-10 and TNF- α were detected by enzyme-linked immunosorbent assay (ELISA). Results: Tanshinone IIA Sodium Sulfonate significantly ameliorated traumatic-hemorrhagic shock resulted in the deterioration of hemodynamics, notably decreased traumatic-hemorrhagic shock resulted in the elevation of inflammatory cytokines. Conclusion: Tanshinone IIA Sodium Sulfonate improved traumatic-hemorrhagic shock induced hypotension, and inhibited traumatic-hemorrhagic shock induced inflammatory response. It may have protective effects on traumatic-hemorrhagic shock, and may offer useful information for treating traumatic-hemorrhagic shock clinically.

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