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氧疗对新生儿肺不良影响的光镜和超微结构研究。

Light microscopic and ultrastructural study of the adverse effects of oxygen therapy on the neonate lung.

作者信息

Anderson W R, Strickland M B, Tsai S H, Haglin J J

出版信息

Am J Pathol. 1973 Nov;73(2):327-48.

PMID:4758788
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1904070/
Abstract

Alterations of lung tissues were evaluated in 74 infants with respiratory distress who received respirator therapy and high concentrations of oxygen for varying durations. Infant survival ranged from 3 hours to 135 days. Sequential pathologic changes were revealed to be an exudative reaction superimposed upon the early stages of typical hyaline membrane disease. This merged with and was eventually replaced by a reparative fibroproliferative response that was most pronounced in those infants who survived for the longest period of time. This response appeared causally related to the development of pulmonary complications of interstitial fibrosis, emphysema, obliterative bronchiolitis and cystic bronchiolectasis. Correlative ultrastructural studies disclosed generalized capillary endothelial damage in early stages of oxygen therapy, interstitial edema and alteration of alveolar cells attributed to the toxic effects of oxygen. Proliferation of type 2 alveolar cells with incorporation of hyaline membranes into septal walls was a notable feature of the reparative reaction and appeared significant in the subsequent development of interstitial fibrosis.

摘要

对74例接受呼吸机治疗并吸入不同时长高浓度氧气的呼吸窘迫婴儿的肺组织改变进行了评估。婴儿存活时间从3小时至135天不等。连续的病理变化显示为典型透明膜病早期叠加的渗出反应。这种反应与修复性纤维增生反应融合,并最终被其取代,这种反应在存活时间最长的婴儿中最为明显。这种反应似乎与间质性纤维化、肺气肿、闭塞性细支气管炎和囊性细支气管扩张等肺部并发症的发生有因果关系。相关的超微结构研究揭示,在氧疗早期存在广泛性毛细血管内皮损伤、间质水肿以及由于氧的毒性作用导致的肺泡细胞改变。Ⅱ型肺泡细胞增殖并将透明膜纳入间隔壁是修复反应的一个显著特征,并且在随后的间质性纤维化发展中似乎具有重要意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e87/1904070/f50e43314614/amjpathol00249-0090-a.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e87/1904070/2f7194ce5c9b/amjpathol00249-0091-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e87/1904070/7648586255b0/amjpathol00249-0092-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e87/1904070/d8f7b0aea236/amjpathol00249-0092-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e87/1904070/0a56915ceec5/amjpathol00249-0093-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e87/1904070/7782b7986e59/amjpathol00249-0093-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e87/1904070/261b915f046f/amjpathol00249-0094-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e87/1904070/5af0c0ac6a32/amjpathol00249-0087-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e87/1904070/dde16db9b328/amjpathol00249-0088-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/1e87/1904070/0a37522f6d49/amjpathol00249-0088-b.jpg
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引用本文的文献

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2
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3
The role of intraalveolar fibrosis in the process of pulmonary structural remodeling in patients with diffuse alveolar damage.肺泡内纤维化在弥漫性肺泡损伤患者肺结构重塑过程中的作用。

本文引用的文献

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The pathological effects due to increase of oxygen tension in the air breathed.由于所呼吸空气中氧分压升高而产生的病理效应。
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High oxygen and hyaline-like membranes.
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Development of fine structural damage to alveolar and capillary lining cells in oxygen-poisoned rat lungs.氧中毒大鼠肺脏中肺泡和毛细血管衬里细胞的超微结构损伤的发展
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Pulmonary lesions associated with oxygen therapy and artificial ventilation.与氧疗和人工通气相关的肺部病变
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Structure of rat lung after protracted oxygen breathing.长时间吸氧后大鼠肺的结构
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