In the acute respiratory distress syndrome (ARDS), alveolar surface tension, T, may be elevated. Elevated T should increase ventilation-induced lung injury. Exogenous surfactant therapy, intended to lower T, has not reduced mortality. Sulforhodamine B (SRB) might, alternatively, be employed to lower T. We test whether substances suspected of elevating T in ARDS raise T in the lungs and test the abilities of exogenous surfactant and SRB to reduce T. In isolated rat lungs, we micropuncture a surface alveolus and instill a solution of a purported T-raising substance: control saline, cell debris, secretory phospholipase A₂ (sPLA₂), acid or mucins. We test each substance alone; with albumin, to model proteinaceous edema liquid; with albumin and exogenous surfactant; or with albumin and SRB. We determine T in situ in the lungs by combining servo-nulling pressure measurement with confocal microscopy, and applying the Laplace relation. With control saline, albumin does not alter T, additional surfactant raises T and additional SRB lowers T. The experimental substances, without or with albumin, raise T. Excepting under aspiration conditions, addition of surfactant or SRB lowers T. Exogenous surfactant activity is concentration and ventilation dependent. Sulforhodamine B, which could be delivered intravascularly, holds promise as an alternative therapeutic.

中文翻译：

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Sulforhodamine B 和外源性表面活性剂对急性呼吸窘迫综合征条件下肺泡表面张力的影响。

在急性呼吸窘迫综合征 (ARDS) 中，肺泡表面张力 T 可能升高。升高的 T 应增加通气引起的肺损伤。旨在降低 T 的外源性表面活性剂疗法并未降低死亡率。Sulforhodamine B (SRB) 也可用于降低 T。我们测试怀疑在 ARDS 中升高 T 的物质是否会提高肺中的 T，并测试外源性表面活性剂和 SRB 降低 T 的能力。在离体的大鼠肺中，我们进行微穿刺表面肺泡并滴注据称的 T 升高物质的溶液：对照盐水、细胞碎片、分泌性磷脂酶 A ₂ (sPLA ₂)、酸或粘蛋白。我们单独测试每种物质；用白蛋白，模拟蛋白质水肿液；含白蛋白和外源性表面活性剂；或与白蛋白和 SRB。我们通过将伺服归零压力测量与共聚焦显微镜相结合并应用拉普拉斯关系来确定肺中的 T 原位。使用对照盐水，白蛋白不会改变 T，额外的表面活性剂会提高 T，额外的 SRB 会降低 T。没有或有白蛋白的实验物质会提高 T。除了在吸入条件下，添加表面活性剂或 SRB 会降低 T。外源性表面活性剂活性是浓度和通风依赖。Sulforhodamine B 可以通过血管内给药，有望作为一种替代疗法。