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高氧性肺损伤及恢复过程中Ⅱ型肺细胞的变化。

Type II pneumocyte changes during hyperoxic lung injury and recovery.

作者信息

Holm B A, Matalon S, Finkelstein J N, Notter R H

机构信息

Department of Biophysics, University of Rochester, New York 14642.

出版信息

J Appl Physiol (1985). 1988 Dec;65(6):2672-8. doi: 10.1152/jappl.1988.65.6.2672.

DOI:10.1152/jappl.1988.65.6.2672
PMID:3215867
Abstract

Adult rabbits exposed to 100% O2 for 64 h and then returned to room air for up to 200 h, develop a lung injury characterized by decreased levels of alveolar surfactant followed by a rebound recovery. In the present study we isolated alveolar type II cells from rabbits at various times during hyperoxic exposure and recovery and measured rates of phosphatidylcholine (PC) synthesis, cellular lipid content, and the specific activity of glycerol 3-phosphate (G-3-P) acyltransferase, an enzyme that catalyzes one of the early reactions in phosphoglyceride biosynthesis. These biochemical parameters were compared with measurements of cell size and cell cycle phase by laser flow cytometry. Results showed that alterations in alveolar phospholipid levels in vivo correlated consistently with cellular lipid metabolic changes measured in isolated type II pneumocytes. In particular, alveolar pneumocytes isolated from lungs of rabbits exposed to 100% O2 for 64 h exhibited a 60% decrease in PC synthesis, cell lipid content, and G-3-P acyltransferase activity. All variables then followed a pattern of recovery to normal and ultimately supranormal levels beginning at approximately 3 days postexposure, at which point there was also a measured increase in the number of type II cells in S phase. These findings suggest that O2-induced changes in type II cell surfactant biosynthesis may account, at least in part, for observed changes in lung phospholipid levels in vivo.

摘要

成年兔暴露于100%氧气中64小时,然后再回到室内空气中长达200小时,会出现以肺泡表面活性物质水平降低为特征的肺损伤,随后会有反弹恢复。在本研究中,我们在高氧暴露和恢复过程中的不同时间从兔体内分离出II型肺泡细胞,并测量磷脂酰胆碱(PC)合成速率、细胞脂质含量以及甘油3 -磷酸(G - 3 - P)酰基转移酶的比活性,该酶催化磷酸甘油酯生物合成中的早期反应之一。通过激光流式细胞术将这些生化参数与细胞大小和细胞周期阶段的测量结果进行比较。结果表明,体内肺泡磷脂水平的变化与在分离的II型肺细胞中测量到的细胞脂质代谢变化始终相关。特别是,从暴露于100%氧气64小时的兔肺中分离出的肺泡细胞,其PC合成、细胞脂质含量和G - 3 - P酰基转移酶活性降低了60%。所有变量随后都呈现出恢复到正常水平并最终超过正常水平的模式,从暴露后约3天开始,此时处于S期的II型细胞数量也有测量到的增加。这些发现表明,氧气诱导的II型细胞表面活性物质生物合成变化可能至少部分解释了体内观察到的肺磷脂水平变化。

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