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目的：探讨不同浓度的一氧化碳（CO）对缺血再灌注后心肌细胞存活率、LDH水平及活性氧（ROS）生成的影响。方法：将H9c2心肌细胞随机分为Sham组，Control组及CORM组。Control组及CORM组为缺血再灌注（氧糖剥夺3h－氧糖恢复1h）后 H9c2细胞。 CORM 组在再灌注开始时分别给予 CO 释放分子2（CORM2）20μM，40μM，60μM，80μM，100μM干预。检测各组细胞存活率、LDH水平及ROS生成。结果：CORM2浓度在20μM，40μM，60μM及80μM时，细胞ROS生成及LDH水平较Control组有明显降低，细胞存活率增加，其中以CORM240μM最为显著。当CORM2浓度为100uM，各项指标与Control组比较无统计学差异。结论：CO在有效低浓度范围内，可减少再灌注损伤心肌细胞ROS的生成，改善细胞损伤。“,”Objective: To investigate the effects of different dosage carbon monoxide (CO) on myocardial cell ROS production, MTT and LDH activity after ischemia-reperfusion injury. Methods: Ischemia/reperfusion model of H9c2 (OGD3h-OGR1h) was established. H9c2 cells were randomly divided into Sham group, Control group, and different dosage CORM groups treated with CORM2 (20 μM, 40 μM, 60 μM, 80 μM, 100 μM) at the onset of reperfusion. H9c2 cell ROS production, MTT and LDH activity were detected. Results: Cell ROS production and LDH activity were significantly decreased and cell viability were evidently increased in CORM (20 μM, 40 μM, 60μM, 80 μM) groups compared with Control group. The effect of CORM40μM was relatively the most remarkable. 100μM CORM2 had no protective effect on H9c2 cells after ischemia-reperfusion. Conclusion: CO in the effective range of low concentration can provide protection to the cardiac cells subjected to ischemia/reperfusion injury by reducing cell ROS production.