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目的：探讨吸入一氧化氮（ＮＯ）对急性呼吸窘迫综合征（ＡＲＤＳ）肺换气功能的影响及其毒副作用。方法：油酸诱发新西兰兔ＡＲＤＳ模型后分组（ｎ＝９）进行机械通气治疗４ｈｒ：（１）对照组；（２）吸入２０ｐｐｍＮＯ（ＮＯ组）。于动物实验的基础状态、治疗前测定ＰａＯ２／ＦｉＯ２、肺内静动脉分流（Ｑ·ｓ／Ｑ·ｔ）、血ＮＯ２－／ＮＯ３－和高铁血红蛋白（ＭｅｔＨｂ），治疗后ＰａＯ２／ＦｉＯ２于１、２、４ｈｒ，其余指标于４ｈｒ复查一次。观察肺病理并测定肺湿干重比（Ｗ／Ｄ）。结果：治疗后，对照组ＰａＯ２／ＦｉＯ２较治疗前呈下降趋势（４ｈｒ，Ｐ＜０．０５），Ｑ·ｓ／Ｑ·ｔ增加（４ｈｒ，Ｐ＜０．０１），ＮＯ组各时点ＰａＯ２／ＦｉＯ２均较治疗前和同时点的对照组明显增加（Ｐ＜０．０１～０．０５），Ｑ·ｓ／Ｑ·ｔ明显低于治疗前和同时点的对照组（４ｈｒ，Ｐ＜０．０５，Ｐ＜０．０１）。实验结束时，ＮＯ组ＮＯ２－／ＮＯ３－和ＭｅｔＨｂ较对照组显著增加（Ｐ＜０．０５，Ｐ＜０．０１），两组的肺病理和Ｗ／Ｄ无明显区别。结论：吸入２０ｐｐｍ能够明显改善兔油酸型ＡＲＤＳ的肺换气功能，无明显近期毒副作用
Objective: To investigate the effects of inhaled nitric oxide (NO) on pulmonary ventilation in acute respiratory distress syndrome (ARDS) and its toxicities and side effects. Methods: New Zealand rabbits were induced by oleic acid ARDS model group (n = 9) for mechanical ventilation for 4 hours: (1) control group; (2) inhalation of 20ppmNO (NO group). PaO2 / FiO2, pulmonary arteriovenous shunt (Q · s / Q · t), blood NO2- / NO3- and methemoglobin (MetHb) were measured in the basal state of the animal experiment. PaO2 / 2,4hr, the remaining indicators in 4hr review time. Lung pathology was observed and lung wet / dry weight ratio (W / D) was measured. Results After treatment, the PaO2 / FiO2 of the control group showed a decreasing trend (4hr, P <0.05) and the Q · s / Qt increased (4hr, P <0.01) / FiO2 were significantly increased (P <0.01 ~ 0.05), Q · s / Q · t was significantly lower than the control group before and at the same time point (4hr, P <0 .05, P <0.01). At the end of the experiment, NO2- / NO3- and MetHb were significantly increased in NO group compared with control group (P <0.05, P <0.01). There was no significant difference between the two groups in lung pathology and W / D. CONCLUSIONS: Inhalation of 20 ppm can significantly improve pulmonary ventilation in rabbit oleic ARDS without any significant recent side effects