Sulforhodamine B and exogenous surfactant effects on alveolar surface tension under acute respiratory distress syndrome conditions.

In the acute respiratory distress syndrome (ARDS), alveolar surface tension, , may be elevated. Elevated should increase ventilation-induced lung injury. Exogenous surfactant therapy, intended to lower , has not reduced mortality. Sulforhodamine B (SRB) might, alternatively, be used to lower . We test whether substances suspected of elevating in ARDS raise in the lungs and test the abilities of exogenous surfactant and SRB to reduce . In isolated rat lungs, we micropuncture a surface alveolus and instill a solution of a purported raising substance: control saline, cell debris, secretory phospholipase A (sPLA), acid, or mucins. We test each substance alone; with albumin, to model proteinaceous edema liquid; with albumin and exogenous surfactant; and with albumin and SRB. We determine 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 , additional surfactant raises , and additional SRB lowers The experimental substances, without or with albumin, raise Excepting under aspiration conditions, addition of surfactant or SRB lowers . Exogenous surfactant activity is concentration and ventilation dependent. Sulforhodamine B, which could be delivered intravascularly, holds promise as an alternative therapeutic. In the acute respiratory distress syndrome (ARDS), lowering surface tension, , should reduce ventilation injury yet exogenous surfactant has not reduced mortality. We show with direct determination in isolated lungs that substances suggested to elevate in ARDS indeed raise , and exogenous surfactant reduces Further, we extend our previous finding that sulforhodamine B (SRB) reduces below normal in healthy lungs and show that SRB, too, reduces under ARDS conditions.