【摘要】 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。更多还原

【Abstract】 AIM:To study whether carbon monoxide serves as a new endogenous mediator taking Part in the pathogenesis ofendotoxin shock RESULTS: The levels of carbon monoxide and nitrite/nitrate in the plasma and aorta were significantly increased in endotoxin shock. The treatment with both heme oxygenase inhibitor zinc protoporphyrin and nitric oxide synthase inhibitopr could significantly reduce the hypotension and metabolic acidosis in endotoxin shock. Zinc Protopor pyrin could significantly decrease the enhancement of carbon monoxide levels in the plasma and aorta but had no effect on nitrite/nitrate levels, whereas dexamethasone could significantly decrease the rise of nitrite/nitrate levels in the plasma but had no influence on carbon monoxide levels. CONCLUSION: Carbon monoxide is a new endogenous mediator in addition to nitric oxide which takes part in the pathophysiology of endotoxin shock.更多还原