The Effect of Nicotinamide on Microcirculatory Function, Tissue Oxygenation and Bioenergetic Status in Rat Tumors

The failure of many attempts to improve tumor oxygenation - and thus the outcome of standard radiotherapy - may be due to the fact that the occurrence of hypoxia in tumors is not solely a result of diffusion-limited “chronic” hypoxia but is also due to temporary flow cessations in microregional tumor perfusion which have been shown to occur in tumor tissue1. As a result, attempts have more recently been made to reduce hypoxia in tumors through the reduction of tumor perfusion fluctuations. The benzamide analog nicotinamide is an agent which has recently received attention in this respect. It has been reported to be an effective, tumor-specific radiosensitizer in several tumor models, an effect thought to be mediated through an increase in tumor blood perfusion2. To date, little is known about the mechanism by which nicotinamide brings about its radiosensitizing effect. The aim of this study therefore was to investigate nicotinamide-induced changes in tumor and muscle microcirculatory function, tumor oxygenation, and tumor and muscle metabolism in an attempt to try and elucidate possible mechanisms for nicotinamide’s actions.