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肺移植相关事件大鼠模型中细胞内表面活性剂池的超微结构变化。

Ultrastructural changes of the intracellular surfactant pool in a rat model of lung transplantation-related events.

机构信息

Institute of Functional and Applied Anatomy, Hannover Medical School, Hannover, Germany.

出版信息

Respir Res. 2011 Jun 14;12(1):79. doi: 10.1186/1465-9921-12-79.

DOI:10.1186/1465-9921-12-79
PMID:21669009
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3125224/
Abstract

BACKGROUND

Ischemia/reperfusion (I/R) injury, involved in primary graft dysfunction following lung transplantation, leads to inactivation of intra-alveolar surfactant which facilitates injury of the blood-air barrier. The alveolar epithelial type II cells (AE2 cells) synthesize, store and secrete surfactant; thus, an intracellular surfactant pool stored in lamellar bodies (Lb) can be distinguished from the intra-alveolar surfactant pool. The aim of this study was to investigate ultrastructural alterations of the intracellular surfactant pool in a model, mimicking transplantation-related procedures including flush perfusion, cold ischemia and reperfusion combined with mechanical ventilation.

METHODS

Using design-based stereology at the light and electron microscopic level, number, surface area and mean volume of AE2 cells as well as number, size and total volume of Lb were determined in a group subjected to transplantation-related procedures including both I/R injury and mechanical ventilation (I/R group) and a control group.

RESULTS

After I/R injury, the mean number of Lb per AE2 cell was significantly reduced compared to the control group, accompanied by a significant increase in the luminal surface area per AE2 cell in the I/R group. This increase in the luminal surface area correlated with the decrease in surface area of Lb per AE2. The number-weighted mean volume of Lb in the I/R group showed a tendency to increase.

CONCLUSION

We suggest that in this animal model the reduction of the number of Lb per AE2 cell is most likely due to stimulated exocytosis of Lb into the alveolar space. The loss of Lb is partly compensated by an increased size of Lb thus maintaining total volume of Lb per AE2 cell and lung. This mechanism counteracts at least in part the inactivation of the intra-alveolar surfactant.

摘要

背景

缺血/再灌注(I/R)损伤是肺移植后原发性移植物功能障碍的原因,导致肺泡表面活性物质失活,从而促进血-气屏障损伤。肺泡上皮 II 型细胞(AE2 细胞)合成、储存和分泌表面活性物质;因此,可以区分存在于板层小体(Lb)中的细胞内表面活性物质池与肺泡内表面活性物质池。本研究旨在研究模拟与移植相关的程序(包括冲洗灌注、冷缺血和再灌注以及机械通气)中,细胞内表面活性物质池的超微结构变化。

方法

在光镜和电子显微镜水平上,采用基于设计的体视学方法,测定经历与移植相关的程序(包括 I/R 损伤和机械通气)的一组和对照组中 AE2 细胞的数量、表面积和平均体积以及 Lb 的数量、大小和总体积。

结果

与对照组相比,I/R 损伤后,每个 AE2 细胞的 Lb 数量明显减少,同时 I/R 组 AE2 细胞的腔表面面积显著增加。腔表面面积的增加与 Lb 表面积与 AE2 的减少有关。I/R 组的 Lb 数加权平均体积呈增加趋势。

结论

我们认为,在这个动物模型中,AE2 细胞中 Lb 的数量减少很可能是由于 Lb 刺激分泌到肺泡腔中。Lb 的丢失部分由 Lb 的大小增加来补偿,从而维持每个 AE2 细胞和肺的 Lb 总容积。这种机制至少部分地对抗了肺泡内表面活性物质的失活。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/480f/3125224/d6635dfb9d0c/1465-9921-12-79-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/480f/3125224/80fe4f2771b5/1465-9921-12-79-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/480f/3125224/48f7645f0106/1465-9921-12-79-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/480f/3125224/2b43c034be30/1465-9921-12-79-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/480f/3125224/48c68f4f4d87/1465-9921-12-79-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/480f/3125224/185ca3735bf8/1465-9921-12-79-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/480f/3125224/d6635dfb9d0c/1465-9921-12-79-6.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/480f/3125224/80fe4f2771b5/1465-9921-12-79-1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/480f/3125224/48f7645f0106/1465-9921-12-79-2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/480f/3125224/2b43c034be30/1465-9921-12-79-3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/480f/3125224/48c68f4f4d87/1465-9921-12-79-4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/480f/3125224/185ca3735bf8/1465-9921-12-79-5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/480f/3125224/d6635dfb9d0c/1465-9921-12-79-6.jpg

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