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本实验采用兔肠系膜上动脉闭塞（ＳＭＡＯ）性休ｋｅ模型，测定了休克前后人．出肺血一氧化氮（ＮＯ）的含量，动态观察了ＮＯ合成抑制剂ＬＮＮＡ对休克时平均动脉血（ＭＡＰ）和肺动脉压（ＰＭＰ）及对生存时间的影响，并测定了人、出肺血脂质过氧化代谢产物丙二醛（ＭＤＡ）的含量改变。结果发现，ＳＭＡＯ休克的出肺血ＮＯ显著低下人肺血（Ｐ＜０．００１），而休克后人、出肺血ＮＯ无明显差异，且与休克前相比也无明显差异。注入Ｌ－ＮＮＡ后显著增加了休克后的ＰＭＰ，缩短了存活时间。并使人、出肺皿ＭＤＡ含量明显增加，结果提示：在兔ＳＭＡＯ休ｋｅ中内源性ＮＯ具有重要的抗肺动脉压增高和抗肺损伤的作用。
In this study, Rabbit superior mesenteric artery occlusion (SMAO) Hugh model, the determination of shock before and after the human. The content of nitric oxide (NO) in pulmonary arteries was measured. The effects of NO synthase inhibitor LNNA on mean arterial blood pressure (MAP) and pulmonary arterial pressure (PMP) and survival time in shock were observed. Changes in the content of malondialdehyde (MDA). The results showed that NO in pulmonary arteries of SMAO shock was significantly lower than that of human pulmonary blood (P <0.001), while there was no significant difference of NO in shock and post-shock in SMAO shock group. The injection of L-NNA significantly increased after shock PMP, shorten the survival time. And the content of MDA in lung and lung was significantly increased. The results suggest that endogenous NO in SMAO-ke ke in rabbits has important anti-pulmonary arterial pressure and anti-lung injury effects.