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目的：探讨一氧化碳(CO)是否作为一种新的内源性介质参与内毒素休克发病机制。结果：血浆以及主动脉CO和一氧化氮（NO）水平在内毒素休克时均显著增高，使用血红素氧合酶抑制剂锌原叶啉和NO合酶抑制剂糖皮质激素地塞米松均可显著减轻内毒素林克中的血压下降和代谢性酸中毒程度，但是锌原卟啉仅能显著抑制血浆以及主动脉CO水平的增高，但对NO2／NO3水平无显著影响；而使用地塞米松则可显著抑制血浆以及主动脉NO2／NO3水平的增高，对CO水平无显著影响。结论：CO是在NO之外的又一个内源性介质，参与内毒素休克一系列病理生理过程。
Objective: To investigate whether carbon monoxide (CO) participates in the pathogenesis of endotoxic shock as a new endogenous mediator. Results: Plasma and aorta CO and nitric oxide (NO) levels were significantly increased during endotoxic shock. Both heme oxygenase inhibitor zinc protoporphyrin and NO synthase inhibitor glucocorticoid dexamethasone However, zinc protoporphyrin could only inhibit the increase of CO level in plasma and aorta, but had no significant effect on the level of NO2 / NO3. However, dexamethasone could reduce the blood pressure and the degree of metabolic acidosis. Significantly inhibited the plasma and aortic NO2 / NO3 levels increased, no significant effect on CO levels. Conclusion: CO is another endogenous mediator besides NO, which is involved in a series of pathophysiological processes of endotoxic shock.