Webster W S, Valois A A
J Neuropathol Exp Neurol. 1981 May;40(3):247-57. doi: 10.1097/00005072-198105000-00003.
Mice (QS outbred strain) received a single subcutaneous injection of cadmium chloride in saline on postnatal day 1, 8, 15, or 22. Histological examination, 24 hours after cadmium exposure on day 1, revealed petechial hemorrhages, edema, and cellular pycnosis throughout much of the immature brain. Treatment on days 8 or 15 produced similar damage, particularly edema and pycnosis, but affected progressively less of the brain until, by day 22, the brain was apparently unaffected by cadmium. Some animals, allowed to survive six to eight weeks after cadmium injection, showed behavioral anomalies and persistent brain deficits. Electron microscopic examination of parietal cortex from animals exposed to cadmium on day 1 revealed that petechial hemorrhages first occurred tow hours after treatment. The hemorrhages increased during the next six hours, and were accompanied by thinning and vacuolization of the capillary walls and widening of interendothelial gaps. In general, such changes were restricted to the partially differentiated capillaries. Degenerative changes in the brain cells were first seen about six hours after cadmium exposure.
小鼠(QS远交系)在出生后第1、8、15或22天接受一次皮下注射氯化镉生理盐水溶液。在第1天镉暴露24小时后的组织学检查显示,在大部分未成熟大脑中出现点状出血、水肿和细胞固缩。在第8天或第15天进行治疗产生了类似的损伤,尤其是水肿和固缩,但对大脑的影响逐渐减小,直到第22天,大脑显然未受镉的影响。一些在注射镉后存活6至8周的动物表现出行为异常和持续的脑功能缺陷。对在第1天暴露于镉的动物的顶叶皮质进行电子显微镜检查发现,点状出血在治疗后两小时首次出现。出血在接下来的6小时内增加,并伴有毛细血管壁变薄和空泡化以及内皮间隙增宽。一般来说,这种变化仅限于部分分化的毛细血管。脑细胞的退行性变化在镉暴露后约6小时首次出现。