The response of the microvascular system to radiation: a review

The microvasculature is a ubiquitous organ system having a major role in the pathogenesis of radiation damage to normal tissues. Although the kinetics of radiation damage to endothelial cells is similar to other tissues (as reflected by Do and Dq) the late effect is a manifestation of injury, not only to the endothelial cell population, but also to the basement membrane. Tissue damage is progressive. The initial expression of radiation injury is an increased permeability leading to changes in the extracellular milieu. There is an irregular proliferation of endothelial cells leading to capillaries of irregular diameter and shape. Fibrous proliferation increases the histohematic barrier and is ultimately reflected in a loss of parenchymal cells. Replacement fibrosis progresses until a steady state is reached where the surviving parenchymal cells can be sustained by the microvasculature. The clinical significance depends on the role of the organ system involved. For patients who have medical conditions which adversely effect the stability of the vascular system (hypertension, diabetes, etc.), the expressions of radiation injury may be more severe and increase the morbidity associated with these diseases. Angiogenesis in granulation tissue is less radiosensitive than in steady-state parenchymal tissues. Wound healing is not significantly affected by commonly used therapeutic doses of irradiation, 40-50 Gy delivered 4-6 weeks preoperatively or postoperatively early in the development of the granulation tissue, but may be complicated where a significant degree of fibrosis has developed. The vascular responses leading to telangiectasia were discussed.