[The gastrointestinal post-irradiation syndrome].

L Mandel, V Svoboda
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Abstract

In the recent years, more attention is paid by radiobiologists to both prevention and therapy of a relatively less studied gastrointestinal postirradiation syndrome (GPS). Moreover, the increase in interest in GPS is motivated with the requirement as to obtain the decrease in action of ionizing radiation on the intestinal mucosa at making radiotherapy of abdominal or pelvic region. The GPS occurs consequently to the affected abdominal region or all the organism with ionizing radiation. Its approximal doses from 10 to 100 Gy (gamma) are critical for the survival of intestinal mucosa, especially that of jejunum and ileum. Under the threshold of a single and total dose from 6 to 10 Gy, the intestinal mucosa may usually regenerate, and the survival depends mainly on the preservation or restoration of hemopoietic activity of blood forming tissues. The main pathogenetic GPS factor resides in the afflication of stem cells of mucosal crypts. The intestinal epithelium stops to be fluently replaced after the irradiation. The motion arrests of epithelial cells from crypts to the apex of villi. The elderly cells undergoes degradation, and after several days the denudation of mucosa occurs with possible distortion of deeper layers of intestinal wall. The intestinal microflora is involved in the pathogenesis both directly and indirectly. Amongst the former events is ranged the invasion of distorted mucosa in compromised both local and systemic immunity. Indirectly, the intestinal microflora is GPS associated by stimulating mitotic activity in crypts, therefore more cells are in the radiosensitive phase. In germ-free animals there is a significant decrease in mitotic activity of crypts, and the migration time of epithelial cells from crypts to the apex villi is twice more prolongated, what induces possible restoration of active center after the irradiation. The GPS also results in disorder of metabolic processes which are conditioned with intestinal mucosa. Its typical manifestation resides in the wash-out of mucus, decreased resorption of nutrients and loss of water and minerals into the intestinal lumen. The GPS-related are another disorders of the organism, those of liver and kidney apparently induced due to the intoxication with catabolic products. The microflora has been stated to be involved in GPS by the experiments on germ-free animals. In the absence of microflora, the survival is greater in duration. After a total pigs irradiation with 10-30 Gy, more than two times survival prolongation occurs. The abdominal irradiation with 12 Gy results to the death of only conventional pigs, whereas those germ-free show a survival.(ABSTRACT TRUNCATED AT 400 WORDS)

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[胃肠道辐照后综合征]。
近年来,研究较少的胃肠道放射后综合征(GPS)的预防和治疗越来越受到放射生物学家的关注。此外,在腹部或骨盆区域进行放射治疗时,需要获得电离辐射对肠粘膜作用的减少,这是对GPS研究兴趣增加的动机。因此,受电离辐射影响的腹部区域或所有生物体都会发生GPS。其约10至100 Gy (γ)的剂量对肠粘膜,特别是空肠和回肠的存活至关重要。在6 ~ 10 Gy的单次和总剂量阈值下,肠黏膜通常可再生,其存活主要依赖于造血组织造血活性的保存或恢复。GPS的主要致病因子存在于粘膜隐窝干细胞的纠缠。辐照后肠上皮停止被顺利替换。上皮细胞从隐窝到绒毛顶端的运动阻滞。老年细胞发生降解,几天后发生粘膜剥落,肠壁较深层可能发生变形。肠道菌群直接或间接参与了其发病机制。在前一种情况中,病变粘膜的侵袭损害了局部和全身免疫。间接地,肠道菌群通过刺激隐窝有丝分裂活动与GPS相关,因此更多的细胞处于放射敏感期。无菌动物的隐窝有丝分裂活性明显降低,上皮细胞从隐窝向绒毛顶端迁移的时间延长了两倍以上,这可能导致辐照后活性中心的恢复。GPS还导致肠道粘膜代谢过程的紊乱。其典型表现是粘液排出,营养物质吸收减少,水和矿物质流失到肠腔。与gps相关的是机体的另一种疾病,肝脏和肾脏的疾病显然是由于分解代谢产物中毒引起的。在无菌动物身上进行的实验表明,微生物群与GPS有关。在没有微生物群的情况下,存活时间更长。总辐照剂量为10-30 Gy后,猪的生存时间延长2倍以上。腹部12 Gy辐照只导致常规猪死亡,而无菌猪存活。(摘要删节为400字)
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