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大鼠中度高氧性肺损伤后肺泡上皮液体清除机制保持完好。

Alveolar epithelial fluid clearance mechanisms are intact after moderate hyperoxic lung injury in rats.

作者信息

Garat C, Meignan M, Matthay M A, Luo D F, Jayr C

机构信息

Department of Physiology and Nuclear Medicine, Hôpital Henri Mondor, Créteil, France.

出版信息

Chest. 1997 May;111(5):1381-8. doi: 10.1378/chest.111.5.1381.

Abstract

The capacity of the alveolar epithelial barrier to remove excess alveolar fluid from the airspaces of the lung was studied in an experimental model of moderate hyperoxic lung injury. Rats were exposed to 100% oxygen for 40 h in an exposure chamber and compared with control animals exposed to room air. Extravascular lung water was calculated gravimetrically. Alveolar and lung liquid clearance were studied over 1 h by instillation of a 5% albumin solution with 1.5 microCi of 125I-labeled albumin (6 mL/kg into both lungs). The concentration of both the unlabeled and labeled albumin was used to calculate alveolar liquid clearance. Hyperoxic rats developed pulmonary edema, with a 33% increase in extravascular lung water to 5.3 +/- 0.1 g of water per gram of dry lung, compared with 4.0 +/- 0.2 g of water per gram of dry lung in control rats (p < 0.05). This degree of edema was associated with a significant increase in the alveolar-arterial oxygen difference (241 +/- 61 vs 124 +/- 14 mm Hg in control animals exposed to room air, p < 0.05). Despite this moderate degree of lung injury, alveolar fluid clearance was normal (30 +/- 3%) compared with control rats (33 +/- 6%). Furthermore, the hyperoxic injured rats responded normally to an exogenous beta-adrenergic agonist (terbutaline, 10(-4) mol/L) with a 67% increase in the rate of alveolar liquid clearance (50 +/- 5%). Thus, in the setting of moderate hyperoxic lung injury, the alveolar epithelial barrier is still capable of removing fluid at a normal rate and responding to beta-adrenergic agonist treatment. These experimental results have potential clinical implications for patients with acute lung injury.

摘要

在中度高氧性肺损伤的实验模型中,研究了肺泡上皮屏障从肺气腔中清除过量肺泡液的能力。将大鼠置于暴露舱中,使其暴露于100%氧气环境40小时,并与暴露于室内空气的对照动物进行比较。通过重量法计算血管外肺水含量。通过向双肺滴注含1.5微居里125I标记白蛋白的5%白蛋白溶液(6毫升/千克),在1小时内研究肺泡和肺液清除情况。使用未标记和标记白蛋白的浓度来计算肺泡液清除率。高氧大鼠出现肺水肿,血管外肺水增加33%,达到每克干肺5.3±0.1克水,而对照大鼠为每克干肺4.0±0.2克水(p<0.05)。这种水肿程度与肺泡-动脉氧分压差显著增加相关(暴露于室内空气的对照动物为124±14毫米汞柱,高氧大鼠为241±61毫米汞柱,p<0.05)。尽管存在这种中度肺损伤,但与对照大鼠(33±6%)相比,肺泡液清除率正常(30±3%)。此外,高氧损伤大鼠对外源性β-肾上腺素能激动剂(特布他林,10^(-4)摩尔/升)反应正常,肺泡液清除率增加67%(50±5%)。因此,在中度高氧性肺损伤情况下,肺泡上皮屏障仍能够以正常速率清除液体,并对β-肾上腺素能激动剂治疗产生反应。这些实验结果对急性肺损伤患者具有潜在的临床意义。

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