目的 :探讨肺缺血再灌注损伤时血红素氧合酶 1(HO 1)的变化规律及意义。方法 :4 0只健康日本大耳白兔随机分成假手术对照 (C)组、肺缺血再灌注 (IR)组、肺缺血再灌注 +氯铁血红素 (H)组和肺缺血再灌注 +锌原卟啉 (Z)组。各组在缺血前后 ,再灌注 1h、2h、3h分别抽血检测一氧化碳血红蛋白 (COHb)浓度 ,实验结束时取肺组织测湿 /干重比 (W/D)、肺泡损伤数 (IAR)、HO酶活力并观察细胞超微结构的改变。结果 :与C组相比 ,IR组COHb浓度随缺血和再灌注时间的延长而逐渐升高 ,H组这种趋势更加明显 ,Z组升高较缓和 ;IR组W/D、IAR升高 ,H组下降而Z组明显增加 ;IR组HO酶活力增加 ,H组上升更加显著而Z组明显降低 ;超微结构显示H组较IR组损伤减轻而Z组加重。结论 :HO 1诱导可能通过一氧化碳 (CO)介导减轻肺缺血再灌注损伤。 Objective: To investigate the changes and significance of heme oxygenase 1 (HO 1) during lung ischemia-reperfusion injury. Methods: Forty healthy Japanese white rabbits were randomly divided into sham operation group (C), lung ischemia reperfusion group (IR), lung ischemia / reperfusion group (H group) and ischemia Perfusion + zinc protoporphyrin (Z) group. The concentrations of COHb in each group were measured before and after ischemia and 1h, 2h and 3h after reperfusion. The wet / dry weight ratio (W / D), the number of alveolar damage (IAR) HO enzyme activity and observe the changes of cell ultrastructure. Results: Compared with group C, the concentration of COHb in IR group increased gradually with the prolongation of ischemia and reperfusion time. This tendency was more obvious in group H and more slowly in group Z. The W / D and IAR in IR group were higher , The H group decreased and the Z group increased significantly. The HO enzyme activity increased in IR group, H group increased more significantly and Z group decreased significantly. The ultrastructure showed that the damage of H group was weaker than that of IR group and the Z group was heavier. CONCLUSION: HO 1 induces the possible reduction of lung ischemia-reperfusion injury through the mediation of carbon monoxide (CO).