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新生儿应激暴露的生物嵌入:一个描述应激诱导早产儿神经发育障碍机制的概念模型。

The biological embedding of neonatal stress exposure: A conceptual model describing the mechanisms of stress-induced neurodevelopmental impairment in preterm infants.

作者信息

Nist Marliese Dion, Harrison Tondi M, Steward Deborah K

机构信息

The Ohio State University College of Nursing, Columbus, Ohio.

出版信息

Res Nurs Health. 2019 Feb;42(1):61-71. doi: 10.1002/nur.21923. Epub 2018 Nov 29.

Abstract

The biological embedding of early life stress exposure may result in life-long neurodevelopmental impairment in preterm infants. Infants hospitalized in the neonatal intensive care unit are exposed to significant experiential, environmental, and physiologic stressors over the course of their extended hospitalization. Stress exposure during the sensitive period of brain development may alter biological processes, including functioning of the immune system, the autonomic nervous system, and the hypothalamic-pituitary-adrenal axis as well as gene expression. These alterations may subsequently affect brain structure and function. Changes to these processes may mediate the relationship between neonatal stress exposure and neurodevelopment in preterm infants and represent potential therapeutic targets to improve long-term outcomes. The purpose of this paper is to introduce a conceptual model, based on published research, that describes the mechanisms mediating stress exposure and neurodevelopment impairment in preterm infants and to provide the theoretical foundation on which to base future descriptive research, intervention studies, and clinical care.

摘要

早期生活应激暴露的生物嵌入可能导致早产儿出现终身神经发育障碍。在新生儿重症监护病房住院的婴儿在延长住院期间会受到重大的体验、环境和生理应激源的影响。大脑发育敏感期的应激暴露可能会改变生物过程,包括免疫系统、自主神经系统、下丘脑 - 垂体 - 肾上腺轴的功能以及基因表达。这些改变随后可能影响脑结构和功能。这些过程的变化可能介导新生儿应激暴露与早产儿神经发育之间的关系,并代表改善长期预后的潜在治疗靶点。本文的目的是引入一个基于已发表研究的概念模型,该模型描述了介导早产儿应激暴露和神经发育障碍的机制,并为未来的描述性研究、干预性研究和临床护理提供理论基础。

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