Blood-Siegfried Jane, Rambaud Caroline, Nyska Abraham, Germolec Dori R
Duke University Medical Center, Durham, North Carolina 27707, USA.
Innate Immun. 2008 Jun;14(3):145-52. doi: 10.1177/1753425908090730.
This study compared pathological findings from a neonatal rat model of sudden death with those from 40 sudden infant death syndrome (SIDS) infants collected at autopsy. In the rat model, influenza A virus was administered intranasally on postnatal day 10, and on day 12 a sublethal, intraperitoneal dose of Escherichia coli endotoxin; mortality was 80%. Tissue samples from the animals and infants were fixed in formaldehyde, embedded in paraffin, and sections stained with hematoxylin and eosin. Tissues from the SIDS specimens were additionally cultured for bacteria and viruses; post-mortem blood samples were evaluated for signs of inflammation. All sections were examined by a pediatric forensic pathologist familiar with SIDS pathology. Comparisons between the rat model and the human SIDS cases revealed that both exhibited gross and microscopic pathology related to organ shock, possibly associated with the presence of endotoxin. Uncompensated shock appeared to be a likely factor that caused death in both infants and rat pups. Response to a shock-inducing event might have played an important role in the events leading to death. The similarities between the neonatal rats and the human cases indicate that further research with the model might elucidate additional aspects of SIDS pathology.
本研究将新生大鼠猝死模型的病理结果与40例尸检时收集的婴儿猝死综合征(SIDS)婴儿的病理结果进行了比较。在大鼠模型中,于出生后第10天经鼻给予甲型流感病毒,并于第12天腹腔注射亚致死剂量的大肠杆菌内毒素;死亡率为80%。将动物和婴儿的组织样本固定于甲醛中,石蜡包埋,切片用苏木精和伊红染色。对SIDS标本的组织进行细菌和病毒培养;对死后血样进行炎症迹象评估。所有切片均由熟悉SIDS病理学的儿科法医病理学家检查。大鼠模型与人类SIDS病例之间的比较显示,两者均表现出与器官休克相关的大体和微观病理学特征,可能与内毒素的存在有关。失代偿性休克似乎是导致婴儿和幼鼠死亡的一个可能因素。对休克诱发事件的反应可能在导致死亡的事件中起了重要作用。新生大鼠与人类病例之间的相似性表明,对该模型的进一步研究可能会阐明SIDS病理学的其他方面。