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正常发育及婴儿猝死综合征中的迷走神经复合体

Vagal nerve complex in normal development and sudden infant death syndrome.

作者信息

Becker L E, Zhang W

机构信息

Department of Pathology, Hospital for Sick Children, Toronto, Ontario, Canada.

出版信息

Can J Neurol Sci. 1996 Feb;23(1):24-33. doi: 10.1017/s0317167100039147.

Abstract

BACKGROUND

Although the pathogenesis of sudden infant death syndrome (SIDS) is not understood, one of the major hypotheses is that a subtle defect in respiratory circuitry is an important underlying factor. The vagus nerve is a critical component of respiratory control, but its neuroanatomic complexity has limited its investigation in human disease.

METHODS

Correlating developmental studies on different parts of the vagus nerve allows a more comprehensive assessment of its maturation process. Comparison of the normal developing vagus nerve with nerves examined in SIDS patients suggests alterations in the nucleus tractus solitarius and dorsal vagal nucleus as well as in the peripheral vagus nerve.

RESULTS AND CONCLUSIONS

The persistence of dendritic spines and lack of appropriate axonal growth implies delays in vagal maturation. Since nodose ganglia can be examined in vitro from autopsy material, perturbation to this system can be explored to evaluate further the mechanism involved in terminal vagal maturation. Although the reason for the delayed vagal maturation in SIDS is not apparent, the presence of astrogliosis in the region of the vagal nuclei is consistent with an exposure to hypoxic-ischemic events some time before death.

摘要

背景

尽管婴儿猝死综合征(SIDS)的发病机制尚不清楚,但主要假说之一是呼吸回路的细微缺陷是一个重要的潜在因素。迷走神经是呼吸控制的关键组成部分,但其神经解剖结构的复杂性限制了对其在人类疾病中的研究。

方法

对迷走神经不同部位的发育研究进行关联,能够更全面地评估其成熟过程。将正常发育的迷走神经与在SIDS患者中检查的神经进行比较,提示孤束核和迷走背核以及外周迷走神经存在改变。

结果与结论

树突棘的持续存在和轴突生长缺乏适当性意味着迷走神经成熟延迟。由于可以从尸检材料中体外检查结节神经节,因此可以探索对该系统的扰动,以进一步评估迷走神经终末成熟所涉及的机制。尽管SIDS中迷走神经成熟延迟的原因尚不清楚,但迷走神经核区域存在星形胶质细胞增生与死亡前一段时间暴露于缺氧缺血事件一致。

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