| The Influence of Propofol on Cell Viability after Reoxygenation in Rat Embryonic Heart H9c2 Cells. |
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Yun Hong Kim |
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Department of Anesthesiology and Pain Medicine, Kangbuk Samsung Hospital, Sungkyunkwan University School of Medicine, Seoul, Korea. yhkim12@yahoo.co.kr |
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| Abstract |
BACKGROUND
Although reperfusion is a salvaging method for an acute myocardial infarction, the act of reperfusion itself can paradoxically result in reactive oxygen species (ROS) mediated myocyte death. Propofol has been reported to remove ROS. This study tested the hypothesis that propofol protects H9c2 cardiomyoblasts against hypoxia/reoxygenation (H/R) injury.
METHODS
For the H/R group of cells, hypoxia was induced by replacing the culture medium with serum-/-glucose free Dulbecco's modified Eagle's medium (DMEM) and by exposing cells to 0.5% O2 for 24 h. Following hypoxia, the cells were reoxygenated. The medium was then replaced with fresh medium for maintenance and propofol (0, 25, 50, 250micrometer) was added to the cells (n = 3 for each concentration). In the normoxia group of cells (n = 3), cells were incubated under 21% O2 for 48 h without propofol. The MTT (3-(4,5 dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide) assay was performed 8 and 24 h after reoxygenation for the H/R group of cells, and 32 and 48 h for the normoxia group of cells. The results of the MTT assay were determined with an ELISA spectrometer at a wavelength of 595 nm.
RESULTS
At 8 and 24 h after reoxygenation, MTT formazans in the H/R group of cells were significantly reduced as compared with the normoxia group of cells (P < 0.05). In the presence of 25, 50 and 250micrometer propofol, the MTT activity at 8 and 24 h after reoxygenation was diminished when compared to exposure to 0micrometer propofol (P < 0.05). However, the formazans produced when cells were exposed to a concentration of 25micrometer in propofol convalesced to the level of 0micrometer propofol at 24 h after reoxygenation.
CONCLUSIONS
These results suggest that propofol may play a role in increasing the number of non-viable cells during reoxygenation of the heart. |
| Key Words:
cell viability; heart; MTT formazan; propofol; reperfusion injury |
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