Microvasculature and radiation damage.

Abstract

The association between late damage in irradiated tissues and the vasculature was reported shortly after the discovery of X-rays. Gross blood vessel abnormalities were a consistent finding in radiation-damaged tissues (Gassmann 1899; Muhsam 1904). Since then there have been numerous pathology reports emphasizing the significance of vascular damage in association with late radiation effects. This led to a hypothesis, to a major degree conceived by Rubin and Casarett (1968), that the vascular system was the main target for late radiation damage in normal tissues, the effects seen being related to vascular insufficiency. Although the validity of this hypothesis has been correctly challenged (Withers et al. 1980), there is still sufficient evidence to implicate the slowly dividing cells in the walls of blood vessels as the target cell populations in the pathogenesis of late radiation effects. Most recently, research related to radiation effects on the vasculature has focused on radiation-induced modifications in endothelial cell clonogenic survival and time-related changes in endothelial cell number. In addition, within the last decade, modifications in endothelial cell function have become more fully understood. Some of the most recent findings have raised the possibility of treating the endothelial-cell-mediated effects, leading to the amelioration of late radiation damage in normal tissues.