地塞米松抑制兔内毒素休克进程中血浆ET 1和NO的异常升高

目的　探讨地塞米松（Ｄｅｘ）抗毒作用原理。方法　兔ｉｖ 内毒素６００ μｇ·ｋｇ－ １ 诱发休克,３０ ｍｉｎ 时分别ｉｖ 生理盐水或Ｄｅｘ 、Ｌ ＮＭＡ、ｐｈｏｓｐｈｏｒａｍｉｄｏｎ （ｐｈｏｓ）, 测平均动脉压（ＭＡＰ） 、每搏心输出量（ＳＶ）、和血浆ＥＴ １ 与ＮＯ－３ 浓度。结果　休克兔血浆ＮＯ－３ 、ＥＴ １ 浓度升高, 血流动力学进行性紊乱直至死亡。Ｌ ＮＭＡ 和Ｐｈｏｓ 分别抑制血浆ＮＯ－３ 或ＥＴ １浓度异常升高及基础分泌,短暂改善血流动力学指标。Ｄｅｘ 不影响ＮＯ、ＥＴ １ 基础水平,但抑制休克时兔血浆ＮＯ－３和ＥＴ １ 异常升高、纠正血流动力学紊乱、提高动物生存率。结论　Ｄｅｘ 抑制休克兔血浆ＮＯ、ＥＴ １ 异常升高, 可能是其抗内毒素休克的重要机制之一

Inhibition of NO and endothelin formation by dexamethasone in rabbit endotoxic shock

AIM To investigate the action mechanism of dexamethasone in treating endotoxic shock. METHODS 24 rabbits were injected iv endotoxin 600 μg·kg -1 to induce endotoxic shock. 30 min later, they were injected iv normal saline (control group), or dexamethasone (Dex) 2 mg·kg -1 , inhibitor of NO synthetase N G Methyl L Arginine ( L NMA) 10 mg·kg -1 , and inhibitor of endothelin converting enzyme phosphoramidon (Phos) 2 mg·kg -1 respectively. The hemodynamic index, plasma nitrate and ET 1 concentrations were measured at regular intervals. RESULTS The results showed that the plasma nitrate and ET 1 concentrations increased obviously, while the hemodynamics progressively deteriorated after endotoxin injection in rabbits. L NMA and Phos inhibited the increases of nitrate or ET 1 respectively, and reduced their baseline levels. The hemodynamics in L NMA and Phos groups were just transiently improved, not soon deteriorated and become indifferent from control group. Dex inhibited the excessive increases of nitrate and ET 1 while did not affect their baseline levels. The hemodynamics was the most steady in Dex group. CONCLUSIONS These data suggested that the antagonism of Dex against the increases of plasma NO and ET 1 during endotoxic shock may be one of the important action mechanism of its anti endotoxic shock.