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目的：通过对脓毒性休克时全身血流动力学及内脏微循环改变的研究，探索新的治疗途径。方法：小型猪２０只，随机分为４ 组：①正常对照组（Ｃ组）：仅给生理盐水；②内毒素组（Ｌ组）：单纯持续泵入内毒素；③Ｎ硝基左旋精氨酸甲酯（Ｌ ＮＡＭＥ）治疗组（ＬＮ 组）：泵入内毒素后１ 小时持续泵入Ｌ ＮＡＭＥ；④Ｌ ＮＡＭＥ对照组（Ｎ 组）：仅给Ｌ ＮＡＭＥ。结果：内毒素持续泵入后１小时，外周（骨骼肌）微循环灌注增高，至４小时末上升约７０％ ；肝、胃、肠等内脏器官微循环灌注急剧下降，至４ 小时末下降约６０％ （Ｐ＜ ０．０５）；门静脉血流量也相应下降。应用一氧化氮合酶（ＮＯＳ）抑制剂Ｌ ＮＡＭＥ后，血浆一氧化氮（ＮＯ）明显下降，ＮＯＳ活性明显减弱，内脏微循环灌注进一步下降。结论：内毒素休克时外周与内脏微循环灌注是不平衡的，内脏微循环灌注急剧下降，血流淤滞为其重要特征。ＮＯＳ抑制剂Ｌ ＮＡＭＥ能提高血压，但不能改善内脏微循环。
OBJECTIVE: To explore new therapeutic approaches through the study of systemic hemodynamics and visceral microcirculation in septic shock. Methods: Twenty mini-pigs were randomly divided into four groups: ① normal control group (group C): only saline; ② endotoxin group (group L): simple continuous infusion of endotoxin; ③ N-nitro-L-arginine L NAME treatment group (LN group): L NAME was pumped into L NAME one hour after the endotoxin was pumped; ④ L NAME control group (N group): L NAME only. Results: 1 hour after the continuous infusion of endotoxin, perfusion of peripheral (skeletal muscle) microcirculation increased to about 70% at the end of 4 hours; microcirculation perfusion of liver, stomach, intestine and other organs decreased sharply to the end of 4 hours 60% (P <0.05); portal vein blood flow decreased accordingly. After nitric oxide synthase (NOS) inhibitor L NAME was applied, plasma nitric oxide (NO) was significantly decreased, NOS activity was significantly decreased, and visceral microcirculation perfusion decreased further. Conclusion: Peripheral and visceral microcirculation perfusion is not balanced during endotoxic shock, and perfusion of visceral microcirculation drops sharply and blood stasis is an important feature. NOS inhibitor L NAME can increase blood pressure, but can not improve visceral microcirculation.