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Journal of the Korean Society for Therapeutic Radiology 1994;12(1): 17-26. |
| Role of Blood Flow vs. O2 Consumption in Nicotinamide-induced Increase pO2 in a Murine Tumor |
| Intae Lee, Moon June Cho, Thomas J Demhartner, Leo E Gerweck |
1Department of Radiation Oncology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.
2Department of Therapeutic Radiology, College of Medicine and Cancer Research Institute, Chungnam National University, Dae-Jeon, Korea. |
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| ABSTRACT |
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We evaluated the effect of nicotinamide on cellular O2 consumption and metabolic status i.e., adenylate phosphates and NAD+ in-vitro, and changes in blood flow in-vivo, to determine whether changes in cellular metabolism or increased oxygen availability, was responsible for increased tumor oxygenation. Thirty min. Pre-incubation of cells with~4mM (=500mg/kg) nicotinamide resulted in no change in cellular O2 consumption. Similarly, neither the adenylate phosphates nor the cellular NAD+ levels were altered in the presence of~4mM nicotinamide. In-vivo, nicotinamide (500mg/kg) increased O2availability as estimated by changes in relative tumor blood flow (RBC flux). The changes in RBC flux measured by the laser Doppler method, were tumor volume dependent and increased from~35% in~150mmdegree tumors to~75% in~500mmdegree tumors. In conclusion, these observations indicate a reduction in local tissue O2 consumption is not a mechanism of improved tumor oxygenation by nicotinamide in FsaII murine tumor model. The primary mechanism of increased pO2 appears to be an increased local tumor blood flow. |
| Key Words:
Nicotinamide, Oxygen consumption (QO2 ), Tumor blood flow (TBF), Laser Doppler flowmetry |
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