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产前大量暴露于原子弹辐射后出现严重智力迟钝。向胎儿大脑的氧转运减少:一种可能的远隔效应机制。

Severe mental retardation after large prenatal exposures to bomb radiation. Reduction in oxygen transport to fetal brain: a possible abscopal mechanism.

作者信息

Mole R H

出版信息

Int J Radiat Biol. 1990 Oct;58(4):705-11. doi: 10.1080/09553009014552051.

Abstract

Reasonable expectations, based on the normal physiology of the human fetus, cast new light on the possibilities of extrapolation from the finding of severe mental retardation (SMR) in Japanese bomb survivors after maternal exposure to 1.8-5.5 Gy T65DR Gy. After such large exposures the fetal haematopoietic tissues (DS86 dose 0.9-2.2 Gy) cannot escape severe damage and a consequent reduction in erythropoiesis. Diminished fetal erythropoiesis will diminish oxygen transport from placenta to fetus. Impaired oxygen transport to the developing forebrain will augment the localized forebrain damage caused directly by large radiation doses. Linear extrapolation of an observed linear dose response for SMR after large radiation exposures is unlikely to be a valid method for predicting the frequency of SMR after much smaller exposures causing minimal damage to the fetal haematopoietic tissues.

摘要

基于人类胎儿的正常生理状况,合理的预期为从日本原子弹爆炸幸存者中母体暴露于1.8 - 5.5戈瑞T65DR戈瑞后出现的严重智力迟钝(SMR)这一发现进行外推的可能性提供了新的线索。在如此大剂量的暴露之后,胎儿造血组织(DS86剂量为0.9 - 2.2戈瑞)无法避免严重损伤,进而导致红细胞生成减少。胎儿红细胞生成减少会减少从胎盘到胎儿的氧气输送。向发育中的前脑的氧气输送受损会加剧由大剂量辐射直接造成的局部前脑损伤。对于大剂量辐射暴露后观察到的SMR线性剂量反应进行线性外推,不太可能是预测对胎儿造血组织造成最小损伤的小得多的暴露后SMR频率的有效方法。

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