BACKGROUND: Reoxygenation of an ischemic heart causes a decrease in the cardiac function, which is known as reperfusion injury that is associated with an increase in the concentration of reactive oxygen species (ROS). This study examined the effect of the propofol concentration on the generation of ROS during reoxygenation in rat embryonic heart H9c2 cells.

METHODS: Cultured H9c2 cells were examined in the following sequences: Prehypoxic, Hypoxic and Reoxygenation period. Each period required 60 minutes. The cells were exposed to propofol at the beginning of the prehypoxic period. Thirty minutes later, DCFH-DA (dichlorofluorescin diacetate) 10 µmeter was added to detect the ROS. The propofol concentrations used were 0, 5, 25, 50, 250 µmeter in the first experiment and 0, 1, 2, 3, 4, 5 µmeter in the second experiment. The ROS level was estimated using a fluorometer at 5-minute intervals from 5 to 60 minutes after reoxygenation.

RESULTS: When the propofol concentrations was > 5 µmeter, the ROS levels were significantly lower than those of the untreated group (P0) (P < 0.05). At propofol concentrations < 5 µmeter, the ROS levels 35 to 60 minutes after reoxygenation were significantly lower that in the untreated group (P < 0.05). Between 5 and 30 minutes after reoxygenation, the cells exposed to 1, 4 and 5 µmeter propofol also showed lower ROS levels than the untreated group P0. However, 2 and 3 µmeter propofol did not show any significant difference in ROS values to those observed in the untreated group except for 2 µmeter at 25 minutes after reoxygenation.

CONCLUSIONS: During the reoxygenation period in H9c2 cells, propofol concentrations > 5 µmeter inhibited ROS production over the whole period, and even 1µmeter showed some inhibition of ROS.