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

Abstract

AbstractIn the acute respiratory distress syndrome (ARDS), alveolar surface tension,T, may be elevated. ElevatedTshould increase ventilation-induced lung injury. Exogenous surfactant therapy, intended to lowerT, has not reduced mortality. Sulforhodamine B (SRB) might, alternatively, be employed to lowerT. We test whether substances suspected of elevatingTin ARDS raiseTin the lungs and test the abilities of exogenous surfactant and SRB to reduceT. In isolated rat lungs, we micropuncture a surface alveolus and instill a solution of a purportedT-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 determineT in situin the lungs by combining servo-nulling pressure measurement with confocal microscopy, and applying the Laplace relation. With control saline, albumin does not alterT, additional surfactant raisesTand additional SRB lowersT. The experimental substances, without or with albumin, raiseT. Excepting under aspiration conditions, addition of surfactant or SRB lowersT. Exogenous surfactant activity is concentration and ventilation dependent. Sulforhodamine B, which could be delivered intravascularly, holds promise as an alternative therapeutic.New and NoteworthyIn the acute respiratory distress syndrome (ARDS), lowering surface tension,T, should reduce ventilation injury yet exogenous surfactant has not reduced mortality. We show with directT-determination in isolated lungs that substances suggested to elevateTin ARDS indeed raiseT, and exogenous surfactant reducesT. Further, we extend our previous finding that sulforhodamine B (SRB) reducesTbelow normal in healthy lungs and show that SRB, too, reducesTunder ARDS conditions.