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幼年和成年大鼠慢性高氧诱导的呼吸可塑性

Respiratory plasticity induced by chronic hyperoxia in juvenile and adult rats.

作者信息

Bavis Ryan W, Danielson Matthew D, Dufour Gemma, Hanus Julia, Pratt Ashley E, Tobin Kristina E

机构信息

Department of Biology, Bates College, Lewiston, ME 04240, USA.

Department of Biology, Bates College, Lewiston, ME 04240, USA.

出版信息

Respir Physiol Neurobiol. 2025 Apr;333:104386. doi: 10.1016/j.resp.2024.104386. Epub 2024 Dec 26.

DOI:10.1016/j.resp.2024.104386
PMID:39732308
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11829821/
Abstract

Chronic hyperoxia during early postnatal development depresses breathing when neonatal rats are returned to room air and causes long-lasting attenuation of the hypoxic ventilatory response (HVR). In contrast, little is known about the control of breathing of juvenile or adult mammals after chronic exposure to moderate hyperoxia later in life. Therefore, Sprague-Dawley rats were exposed to 60 % O for 7 days (juveniles) or for 4 and 14 days (adults) and ventilation was measured by whole-body plethysmography immediately after the exposure or following a longer period of recovery in room air. Hyperoxia-treated juvenile rats appeared to hypoventilate when returned to room air (11-13 % lower ventilation and CO convection requirement relative to age-matched controls), but chronic hyperoxia did not alter normoxic ventilation in adult rats. In contrast, pre-treatment with chronic hyperoxia augmented the HVR in both juvenile rats (+41 %) and adult rats (+28-50 %). The hypercapnic ventilatory response (7 % CO) also tended to be augmented in adult rats after 14 days of hyperoxia, but this effect was not significant after accounting for variation in metabolic rate (i.e, CO convection requirement). These findings confirm that chronic hyperoxia elicits age-specific respiratory plasticity in rats. These age-dependent differences are not caused by a lack of plasticity in adult-exposed rats; rather, there are qualitative differences in the plasticity that is expressed after chronic hyperoxia in neonates, juveniles, and adults as well as differences in its persistence.

摘要

出生后早期发育阶段的慢性高氧环境,在新生大鼠回到正常空气环境时会抑制呼吸,并导致低氧通气反应(HVR)长期减弱。相比之下,对于幼年或成年哺乳动物在生命后期长期暴露于中度高氧环境后的呼吸控制情况,我们了解甚少。因此,将斯普拉格-道利大鼠暴露于60%氧气环境中7天(幼年大鼠)或4天和14天(成年大鼠),在暴露后或在正常空气中经过较长恢复时间后,通过全身体积描记法测量通气情况。经高氧处理的幼年大鼠回到正常空气环境时似乎出现通气不足(相对于年龄匹配的对照组,通气量和二氧化碳传输需求降低11%-13%),但慢性高氧并未改变成年大鼠的常氧通气。相反,慢性高氧预处理增强了幼年大鼠(增加41%)和成年大鼠(增加28%-50%)的HVR。在成年大鼠中,高氧处理14天后,高碳酸通气反应(7%二氧化碳)也有增强趋势,但在考虑代谢率变化(即二氧化碳传输需求)后,这种影响并不显著。这些发现证实,慢性高氧在大鼠中引发了年龄特异性的呼吸可塑性。这些年龄依赖性差异并非由成年大鼠缺乏可塑性所致;相反,新生儿、幼年和成年大鼠在慢性高氧后所表现出的可塑性存在质的差异,以及其持续性的差异。

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