Powers B E, Gillette E L, Gillette S L, LeCouteur R A, Withrow S J
Department of Radiology and Radiation Biology, Colorado State University, Fort Collins 80523.
Int J Radiat Oncol Biol Phys. 1991 Mar;20(3):463-71. doi: 10.1016/0360-3016(91)90058-c.
The paraaortic region of beagle dogs was irradiated to 15 to 55 Gy intraoperative irradiation, 10 to 47.5 Gy intraoperative irradiation following 50 Gy external beam irradiation in 25 fractions, or 50 to 80 Gy external beam irradiation in 30 fractions. Six MeV electrons were used for intraoperative irradiation, and external beam irradiation was done using photons from a 6 MV linear accelerator. The psoas muscle in the irradiation field was examined histomorphometrically 2 or 5 years after irradiation. The percentage of muscle fibers and capillaries decreased, whereas the percentage of connective tissue increased with increased dose for both intraoperative irradiation only and intraoperative irradiation plus external beam irradiation. The dose causing a 50% decrease in the percentage of muscle fibers was 21.2 Gy and 33.8 Gy at 2 and 5 years, respectively, after intraoperative irradiation alone, and 22.9 Gy and 25.2 Gy at 2 and 5 years, respectively, after intraoperative irradiation combined with 50 Gy external beam irradiation. The ED50 for severe vessel lesions was 19.2 Gy and 25.8 Gy at 2 and 5 years, respectively, after intraoperative irradiation alone and 16.0 Gy and 18.0 Gy at 2 and 5 years, respectively, after intraoperative irradiation combined with 50 Gy external beam irradiation. External beam irradiation alone caused a slight decrease in percentage of muscle fibers with increased dose, and vessel lesions were infrequent or mild. Radiation-induced muscle injury was characterized by loss of muscle fibers, decreased fiber size, severe vessel lesions, hemorrhage, inflammation, coagulation necrosis, and fibrosis. These histopathologic characteristics distinguish this muscle injury from that caused by neurogenic atrophy. These data indicate that radiation-induced muscle injury most likely was caused by injury of the supporting vasculature. The lesions produced were largely a function of the single intraoperative dose rather than the external beam fractionated doses. Furthermore, it appears that 20 to 25 Gy intraoperative irradiation combined with 50 Gy external beam irradiation may be near the maximum tolerated dose by sublumbar musculature and its supporting vasculature.
对比格犬的主动脉旁区域进行术中照射,剂量为15至55 Gy,或在25次分割的50 Gy外照射后进行10至47.5 Gy术中照射,或在30次分割中进行50至80 Gy外照射。术中照射使用6 MeV电子,外照射使用6 MV直线加速器产生的光子。在照射后2年或5年,对照射野内的腰大肌进行组织形态计量学检查。仅术中照射以及术中照射加外照射时,随着剂量增加,肌纤维和毛细血管的百分比均下降,而结缔组织的百分比增加。仅术中照射后,导致肌纤维百分比下降50%的剂量在2年和5年时分别为21.2 Gy和33.8 Gy,术中照射联合50 Gy外照射后,在2年和5年时分别为22.9 Gy和25.2 Gy。仅术中照射后,严重血管病变的半数有效剂量(ED50)在2年和5年时分别为19.2 Gy和25.8 Gy,术中照射联合50 Gy外照射后,在2年和5年时分别为16.0 Gy和18.0 Gy。单独外照射时,随着剂量增加,肌纤维百分比略有下降,血管病变少见或较轻。辐射诱导的肌肉损伤表现为肌纤维丧失、纤维大小减小、严重血管病变、出血、炎症、凝固性坏死和纤维化。这些组织病理学特征将这种肌肉损伤与神经源性萎缩引起的损伤区分开来。这些数据表明,辐射诱导的肌肉损伤很可能是由支持性脉管系统损伤所致。产生的病变在很大程度上取决于术中单次剂量,而非外照射的分次剂量。此外似乎20至25 Gy术中照射联合50 Gy外照射可能接近腰下肌肉及其支持性脉管系统的最大耐受剂量。