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麻醉绵羊中胸腔积液与通透性增加型肺水肿的关系

Relationship of pleural effusions to increased permeability pulmonary edema in anesthetized sheep.

作者信息

Wiener-Kronish J P, Broaddus V C, Albertine K H, Gropper M A, Matthay M A, Staub N C

机构信息

Cardiovascular Research Institute, University of California, San Francisco 94143-0130.

出版信息

J Clin Invest. 1988 Oct;82(4):1422-9. doi: 10.1172/JCI113747.

Abstract

We studied anesthetized sheep to determine the relationship between increased permeability pulmonary edema and the development and mechanism of pleural effusion formation. In 12 sheep with intact, closed thoraces, we studied the time course of pleural liquid formation after 0.12 ml/kg i.v. oleic acid. After 1 h, there were no pleural effusions, even though extravascular lung water increased 50% to 6.0 +/- 0.7 g/g dry lung. By 3 h pleural effusions had formed, they reached a maximum at 5 h (48.5 +/- 16.9 ml/thorax), and at 8 h there was no additional accumulation of pleural liquid (45.5 +/- 16.9 ml). Morphologic studies by light and electron microscopy demonstrated subpleural edema but no detectable injury to the visceral pleura, suggesting that the pleural liquid originated from the lung and not the pleura. In nine sheep, we quantified the rate of formation of pleural liquid by enclosing one lung in a plastic bag. By comparing in the same sheep the volume of pleural liquid collected from the enclosed lung to the volume found in the opposite intact chest, we estimated the rate of liquid absorption from the intact chest to be 0.32 ml/(kg.h); we had previously reported a liquid absorption rate of 0.28 ml/(kg.h) in normal sheep. These studies also supported the conclusion that the majority of the pleural liquid originated from the lung because we could account for all of the pleural liquid that was formed and cleared. The volume of pleural liquid collected from the enclosed lungs was equal to 21% of the excess lung liquid that formed after oleic acid-induced lung injury. Thus, the pleural space and parietal pleural lymphatic pathways are important pathways for the clearance of pulmonary edema liquid after experimentally induced increased permeability pulmonary edema.

摘要

我们对麻醉的绵羊进行了研究,以确定通透性增加性肺水肿与胸腔积液形成的发展及机制之间的关系。在12只胸廓完整且封闭的绵羊中,我们研究了静脉注射0.12 ml/kg油酸后胸腔积液形成的时间进程。1小时后,尽管血管外肺水增加了50%,达到6.0±0.7 g/g干肺,但并未出现胸腔积液。到3小时时形成了胸腔积液,在5小时时达到最大值(48.5±16.9 ml/胸腔),8小时时胸腔积液没有进一步积聚(45.5±16.9 ml)。光镜和电镜形态学研究显示胸膜下水肿,但未发现脏层胸膜有可检测到的损伤,这表明胸腔积液源自肺而非胸膜。在9只绵羊中,我们通过将一侧肺装入塑料袋来量化胸腔积液的形成速率。通过比较同一只绵羊中从封闭肺收集的胸腔积液量与对侧完整胸腔中的积液量,我们估计完整胸腔中液体的吸收速率为0.32 ml/(kg·h);我们之前报道正常绵羊的液体吸收速率为0.28 ml/(kg·h)。这些研究也支持了这样的结论,即大部分胸腔积液源自肺,因为我们能够解释所有形成和清除的胸腔积液。从封闭肺收集的胸腔积液量相当于油酸诱导肺损伤后形成的多余肺液的21%。因此,胸腔和壁层胸膜淋巴途径是实验性诱导的通透性增加性肺水肿后肺水肿液清除的重要途径。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/7708/442700/093c7b599c35/jcinvest00101-0280-a.jpg

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