E. Kallfass et al., EARLY INFLAMMATORY REACTION OF THE RABBIT CELIAC ARTERY WALL AFTER COMBINED INTRAOPERATIVE (IORT) AND EXTERNAL (ERT) IRRADIATION, Radiotherapy and oncology, 39(2), 1996, pp. 167-178
Citations number
54
Categorie Soggetti
Oncology,"Radiology,Nuclear Medicine & Medical Imaging
The present immunohistochemical study of radiation-induced damage in m
ajor blood vessels is based on a multidisciplinary study (Schultz-Hect
or et al., Radiother. Oncol., 38:205-214, 1996) investigating the comb
ined effect of IORT of the coeliac axis and upper abdominal ERT. The p
aper describes the sequential changes occurring in the coeliac artery
after IORT with 30 Gy, i.e. during and after combined IORT and fractio
nated ERT (total dose 40 Gy). Within 24 h after IORT, the arterial wal
l was found to be invaded by TNF-alpha positive macrophages, which lat
er on disappeared within 7-14 days. At 2 days post-IORT, the medial sm
ooth muscle cells were strongly positive for TNF-alpha and remained po
sitive throughout the observation period of 63 days. At 80 days, a com
parison of different IORT dose groups showed that TNF-alpha expression
after 20 and 30 Gy IORT plus 40 Gy ERT had subsided, while it was sti
ll strongly evident after 40 Gy IORT. Negative reactions in sham irrad
iated animals or animals treated with ERT alone indicate that TNF-alph
a expression was caused by IORT. After >30 days post-IORT, there was i
ncreased collagen type I deposition in the adventitia. In two animals
receiving the full ERT course, intimal proliferations involving mainly
smooth muscle cells were observed. Our findings indicate that some fe
atures typical of radiation induced arteriosclerosis such as periarter
ial fibrosis and intimal proliferations can occur as early as <60 days
postirradiation. Macrophage invasion as well as TNF-alpha expression
in medial smooth muscle cells are known to be important steps in the d
evelopment of spontaneous atherosclerotic lesions. Therefore, early TN
F-alpha induction in the arterial wall by a high local dose of X-irrad
iation may be regarded as one initiating factor of chronic radiation-i
nduced arteriosclerosis.