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急性肺水肿中肺泡灌洗的机制。

Mechanism of alveolar flooding in acute pulmonary oedema.

作者信息

Staub N C, Gee M, Vreim C

出版信息

Ciba Found Symp. 1976(38):255-72. doi: 10.1002/9780470720202.ch15.

DOI:10.1002/9780470720202.ch15
PMID:1047639
Abstract

In severe pulmonary oedema, the alveoli fill rapidly with fluid of essentially the same protein composition as free interstitial fluid. The usual explanation is that the normally 'tight' alveolar epithelial intercellular junctions suddenly become freely permeable to proteins. But the pathophysiological basis for such a change is unknown. In seven anaesthetized dogs one lower lobe was filled with iso-osmotic fluid containing 125I-labelled albumin. The calculated alveolus-blood albumin permeability over three hours averaged 0.06 X 10(-7) cm/s. It decreased nearly 50% when the alveolar tracer concentration was tripled for three more hours. At autopsy, large interstitial free fluid cuffs around blood vessels and airways were found. Isolated lung lobes were filled with isosmotic fluid containing tracer albumin at 10 and 20 cmH2O (0.98-1.96 kPa) airway pressure. Free interstitial fluid cuffs developed within 30 and 10 minutes, respectively. The tracer protein concentration in the cuff fluid averaged 0.9 that of the alveolar fluid. It is postulated that the terminal airway epithelium is normally permeable to protein and water. In acute pulmonary oedema alveolar flooding may occur along the same pathway after the loose interstitial tissue space is fluid-filled and its pressure exceeds that in the airway. The anatomical site of the bulk fluid and protein leak has not been identified.

摘要

在严重肺水肿时,肺泡迅速被蛋白质成分与游离间质液基本相同的液体充满。通常的解释是,正常情况下“紧密”的肺泡上皮细胞间连接突然对蛋白质变得自由通透。但这种变化的病理生理基础尚不清楚。在7只麻醉犬中,一个下叶被充满含125I标记白蛋白的等渗液。计算得出的三小时内肺泡-血液白蛋白通透性平均为0.06×10(-7)厘米/秒。当肺泡示踪剂浓度在接下来的三小时内增加两倍时,它下降了近50%。尸检时,发现血管和气道周围有大量间质游离液袖套。在气道压力为10和20厘米水柱(0.98 - 1.96千帕)时,将离体肺叶充满含示踪白蛋白的等渗液。分别在30分钟和10分钟内出现了游离间质液袖套。袖套液中的示踪蛋白浓度平均为肺泡液的0.9倍。据推测,终末气道上皮通常对蛋白质和水是通透的。在急性肺水肿时,当疏松的间质组织间隙充满液体且其压力超过气道压力后,肺泡灌流可能沿相同途径发生。大量液体和蛋白质渗漏的解剖部位尚未确定。

相似文献

1
Mechanism of alveolar flooding in acute pulmonary oedema.急性肺水肿中肺泡灌洗的机制。
Ciba Found Symp. 1976(38):255-72. doi: 10.1002/9780470720202.ch15.
2
Role of bulk fluid flow in protein permeability of the dog lung alveolar membrane.大量液体流动在犬肺肺泡膜蛋白质通透性中的作用。
J Appl Physiol Respir Environ Exerc Physiol. 1977 Feb;42(2):144-9. doi: 10.1152/jappl.1977.42.2.144.
3
Protein composition of lung fluids in acute alloxan edema in dogs.犬急性四氧嘧啶性肺水肿肺液的蛋白质组成
Am J Physiol. 1976 Feb;230(2):376-9. doi: 10.1152/ajplegacy.1976.230.2.376.
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Relationships among lung extravascular fluid compartments with alveolar flooding.肺血管外液腔隙与肺泡灌洗之间的关系。
J Appl Physiol Respir Environ Exerc Physiol. 1982 Jul;53(1):267-71. doi: 10.1152/jappl.1982.53.1.267.
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Airway level at which edema liquid enters the air space of isolated dog lungs.水肿液进入离体犬肺气腔的气道水平。
J Appl Physiol (1985). 1989 Dec;67(6):2234-42. doi: 10.1152/jappl.1989.67.6.2234.
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Protein composition of lung fluids in anesthetized dogs with acute cardiogenic edema.急性心源性水肿麻醉犬肺液的蛋白质组成
Am J Physiol. 1976 Nov;231(5 Pt. 1):1466-9. doi: 10.1152/ajplegacy.1976.231.5.1466.
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Alveolar pressure in fluid-filled occluded lung segments during permeability edema.通透性肺水肿时液体充盈的肺闭塞节段中的肺泡压。
J Appl Physiol Respir Environ Exerc Physiol. 1983 Oct;55(4):1098-102. doi: 10.1152/jappl.1983.55.4.1098.
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The permeability of lung capillary and alveolar walls as determinants of liquid movements in the lung.肺毛细血管和肺泡壁的通透性作为肺内液体流动的决定因素。
Ciba Found Symp. 1976(38):49-64. doi: 10.1002/9780470720202.ch4.
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Phenotypic heterogeneity in lung capillary and extra-alveolar endothelial cells. Increased extra-alveolar endothelial permeability is sufficient to decrease compliance.肺毛细血管和肺泡外内皮细胞的表型异质性。肺泡外内皮通透性增加足以降低顺应性。
J Surg Res. 2007 Nov;143(1):70-7. doi: 10.1016/j.jss.2007.03.047.
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Interstitial albumin concentration measured during growth of perivascular cuffs in liquid-filled rabbit lung.在充满液体的兔肺中血管周围套囊生长过程中测量的间质白蛋白浓度。
J Appl Physiol (1985). 2004 Jan;96(1):283-92. doi: 10.1152/japplphysiol.00581.2003.

引用本文的文献

1
Clara cell protein (CC16), a marker of lung epithelial injury, is decreased in plasma and pulmonary edema fluid from patients with acute lung injury.克拉拉细胞蛋白(CC16)是肺上皮损伤的标志物,在急性肺损伤患者的血浆和肺水肿液中含量降低。
Chest. 2009 Jun;135(6):1440-1447. doi: 10.1378/chest.08-2465. Epub 2009 Feb 2.
2
Chemical modulation of alveolar epithelial permeability.肺泡上皮通透性的化学调节
Environ Health Perspect. 1980 Apr;35:13-20. doi: 10.1289/ehp.803513.
3
Therapy of ARDS: positive end-expiratory pressure.急性呼吸窘迫综合征的治疗:呼气末正压通气
West J Med. 1979 Mar;130(3):229-35.