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目的为探讨一氧化氮(NO)在失血性休克中的效应及其意义。方法复制家兔失血性休克模型,动态监测血浆亚硝酸盐(NO-2)活性,以此作为NO含量,同时分别测定血浆丙二醛(MDA)浓度和超氧化物歧化酶(SOD)含量。结果A组动物于休克后lh血浆NO-2活性最高,与组间休克前和B同时相比较有显著性差异(P<005)。血浆SOD含量于休克后lh和MDA浓度休克后4h和8h最高。A组动物于休克后lh血浆NO-2含量与同时相SOD含量呈正相关(r=0637,P<005),与4h和8h同时相MDA含量均呈正相关(r分别为0640和0647,P<005),与休克后1h同时相血压呈负相关(r=-0725,P<001)。结论失血性休克时过量产生的NO可直接扩张血管,降低血管阻力,使血压进一步下降。血浆NO-2、MDA和SOD浓度三者之间在休克时的关系,其确切机制目前尚不十分清楚,有待进一步深入研究
Objective To investigate the effect and significance of nitric oxide (NO) in hemorrhagic shock. Methods Rabbit hemorrhagic shock model was duplicated and the activity of plasma nitrite (NO-2) was dynamically monitored. The content of NO was measured and the content of plasma malondialdehyde (MDA) and the content of superoxide dismutase (SOD) were measured respectively. Results The plasma NO-2 level in group A was the highest at 1 h after shock, which was significantly different from that before shock and at group B (P <005). Plasma SOD content in shock after lh and MDA concentrations shock 4h and 8h after the highest. There was a positive correlation between plasma NO-2 level and SOD level in group A at 1h after shock (r = 0637, P <005), and positive correlation with MDA content at 4h and 8h (r = 00 640 and 0647, respectively, P <005), which was negatively correlated with the same blood pressure at 1 hour after shock (r = -0.725, P <001). Conclusion Overproduction of NO during hemorrhagic shock can directly dilate blood vessels, decrease vascular resistance and further decrease blood pressure. The exact mechanism of the relationship between plasma concentrations of NO-2, MDA and SOD at the time of shock is not yet clear and needs further study