Ruisi Phillip, Ruisi Michael
North Shore University Hospital, Manhasset, and Beth Israel Medical Center, New York, NY, USA.
South Med J. 2011 Jan;104(1):46-8. doi: 10.1097/SMJ.0b013e3181fd7f69.
Carbon monoxide (CO) has been widely recognized as an exogenous poison, although endogenous mechanisms for its formation involve heme-oxygenase (HO) isoforms, more specifically HO-1, in the setting of oxidative stress such as acute respiratory distress syndrome, sepsis, trauma, and nitric oxide use have been studied. In patients with refractory hypoxemia, inhaled nitric oxide (iNO) therapy is used to selectively vasodilate the pulmonary vasculature and improve ventilation-perfusion match. Inhaled nitric oxide is rapidly inactivated on binding to hemoglobin in the formation of nitrosyl- and methemoglobin in the pulmonary vasculature. Hence, inhaled nitric oxide has minimal systemic dissemination. Several experimental design studies involving lab rats have demonstrated increased levels of carboxyhemoglobin and exhaled CO as a result of nitric oxide HO-1 induction.
一氧化碳（CO）一直被广泛认为是一种外源性毒物，尽管其形成的内源性机制涉及血红素加氧酶（HO）亚型，更具体地说是HO-1，在诸如急性呼吸窘迫综合征、脓毒症、创伤和使用一氧化氮等氧化应激情况下，这一机制已得到研究。在难治性低氧血症患者中，吸入一氧化氮（iNO）疗法用于选择性地扩张肺血管并改善通气-灌注匹配。吸入的一氧化氮在肺血管中与血红蛋白结合形成亚硝基血红蛋白和高铁血红蛋白时会迅速失活。因此，吸入的一氧化氮极少会扩散至全身。几项涉及实验大鼠的实验设计研究表明，一氧化氮诱导HO-1会导致碳氧血红蛋白水平和呼出的CO增加。
