摘要目的：探讨地塞米松对失血性休克-再灌注损伤的防治作用。方法：制备家兔失血性休克模型，随机分为地塞米松保护组(Ⅱ组)和未用地塞米松对照组(Ⅰ组)，检测血浆和组织一氧化氮代谢产物(NOP)、丙二醛(MDA)含量及平均动脉压(MAP)。结果：休克前2组动物NOP、MDA及MAP间均无统计学差异。休克90分钟时2组动物NOP、MDA均明显升高，MAP均显著下降。再灌注后，Ⅱ组NOP及MDA均逐渐下降，再灌注3小时后接近休克前水平，但明显低于休克90分钟和Ⅰ组同时间点水平；Ⅱ组MAP逐渐上升，再灌注3小时后接近休克前水平，但明显高于休克90分钟和Ⅰ组同时间点水平。此外，Ⅱ组心、肺、肝、肾、肠道组织NOP及MDA含量均明显低于Ⅰ组。结论：地塞米松可降低一氧化氮及氧自由基水平，减轻脂质过氧化反应，对休克-再灌注损伤起良好的防护作用。

abstractsObjective:To investigate the protective effect of dexamethasone (DXM) on reperfusion injury induced by hemorrhagic shock in rabbits.Methods:Using a hemorrhagic shock model,20 rabbits were randomly divided into non-treatment group (groupⅠ) and treatment group (group Ⅱ),10 rabbits in each group.Rabbits in group Ⅱ DXM (20 mg/kg) was intravenously administrated immediately after reperfusion,while rabbits of the groupⅠ received the same volume of normal saline.Plasma and tissue nitric oxide products (NO,NO－２/NO－３),malonyldialdehyde (MDA) and mean arterial pressure (MAP) were measured before shock,90 minutes of shock and 60,120,180 minutes after reperfusion,respectively.Results:Baseline measurements of NO,MDA and MAP were similar in two groups.90 minutes after hemorrhage,plasma NO and MDA contents significantly increased and MAP values remarkably decreased in both groups as compared to baseline values (all P<0.01 vs.baseline).After treatment with DXM,NO and MDA levels gradually decreased and had a tendency approaching baseline values at 3 hours after reperfusion,which were significantly lower than that of 90 minutes hemorrhage and groupⅠ.In group Ⅱ,MAP increased after reperfusion,at 3 hours,and it was markedly higher than that of 90 minutes hemorrhage and group Ⅰ.In addition,NO and MDA levels in the heart,lung,liver,kidney and intestine in group Ⅱ were lower than those in groupⅠ.Conclusions:DXM could effectively protect vital organs from reperfusion injury following hemorrhagic shock by reducing levels of NO and oxygen free radicals,attenuating lipid peroxidation.