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大鼠创伤性休克后血清一氧化氮的动态变化及其机制 被引量:17

Dynamic changes in serum level of nitric oxide and its mechanisms in rats with traumatic shock
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摘要 目的探讨创伤性休克后血清一氧化氮(NO)浓度的动态变化及其机制。方法通过外力致鼠双侧后肢骨折,制作创伤性休克模型,Griess法测定休克过程中多时间点血清NO3-/ NO2-浓度。结果休克过程中血清NO无明显变化,复苏后早期(1 h)显著下降,6 h达峰值,其后血清NO维持较高水平,24 h仍显著升高。休克未复苏鼠血清NO无显著变化。结论创伤性休克时血中NO无显著变化,复苏后先有一过性NO减少,继而血中NO升高,持续至24 h,再灌注损伤是复苏后期NO合成增多的重要原因。 Objective To investigate the dynamic changes of serum nitric oxide (NO) level and its mechanisms in rats in traumatic shock. Methods Rat models of traumatic shock were established by fracturing the posterior limb of the rats. Serum levels of nitrate/nitrite were measured with the method described by Griess. Results No significant changes in serum NO level took place during traumatic shock. One hour after resuscitation, however, serum NO level first underwent marked decline and then increased to the peak level at 6 h after resuscitation, retaining a high level till 24 h after resuscitation. No obvious changes of serum NO levels were observed in rats without resuscitation. Conclusion Serum NO level does not significantly alter during traumatic shock, while after resuscitation, NO level increases after transient decrease, possibly due to reperfusion injury.
出处 《第一军医大学学报》 CSCD 北大核心 2002年第10期891-894,共4页 Journal of First Military Medical University
基金 广东省自然科学基金(001048)
关键词 休克 创伤性 一氧化氮 shock, traumatic nitric oxide
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  • 1[1]Kirkeboen KA, Strand OA. The role of nitric oxide in sepsis an overview[J]. Acta Anaesthesiol Scand, 1999, 43(3): 275-88.
  • 2[2]Szabo C, Thiemermann C. Invited opinion: role of nitric oxide in hemorrhagic, traumatic, and anaphylactic shock and thermal injury [J]. Shock, 1994, 2(2): 145-55.
  • 3[3]Yao YM, Bahrami S, Leichtfried G, et al. Significance of NO in hemorrhage-induced hemodynamic alterations, organ injury, and mortality in rats[J]. Am J Physiol, 1996, 270(5 Pt 2): 1616-23.
  • 4[4]Goris RJ. Pathophysiology of shock in trauma[J]. Eur J Surg, 2000,166(1): 100-11.
  • 5[5]Schlag G, Redl H. Shock, sepsis and organ failure-nitric oxide[M].Germany: Springer-Verlag Berlin Heidelberg, 1995.84-96.
  • 6[6]Smail N, Catanla R A, Wang P, et al. Gut and liver: the organs responsible for increased nitric oxide production after trauma-hemor-rhage and resuscitation[J]. Arch Surg, 1998, 133(4): 399-405.
  • 7[7]Gebhard F, Nussler AK, Rosch M, et al. Early posttraumatic increase in production of nitric oxide in humans[J]. Shock, 1998, 10(4):237-42.
  • 8[8]Hansen PR. Inflammatory alterations in the myocardial microcirculation[J ]. J Mol Cell Cardiol, 1998, 30(12): 2555-9.
  • 9[9]Delonca J, Balteaux V, Giraud T, et al. EDRF/NO and endothelial functions[J]. Arch Mal Coeur Vaiss, 1993, 86(11): 1617-24.
  • 10[10]Carden DL, Granger DN. Pathophysiology of ischaemia-reperfusion injury[J]. J Pathol, 2000,190(3): 255-66.

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