Surface tension in situ in flooded alveolus unaltered by albumin

Abstract

Kharge AB, Wu Y, Perlman CE. Surface tension in situ in flooded alveolus unaltered by albumin. J Appl Physiol 117: 440 -451, 2014. First published June 26, 2014 doi:10.1152/japplphysiol.00084.2014.-In the acute respiratory distress syndrome, plasma proteins in alveolar edema liquid are thought to inactivate lung surfactant and raise surface tension, T. However, plasma protein-surfactant interaction has been assessed only in vitro, during unphysiologically large surface area compression (%⌬A). Here, we investigate whether plasma proteins raise T in situ in the isolated rat lung under physiologic conditions. We flood alveoli with liquid that omits/includes plasma proteins. We ventilate the lung between transpulmonary pressures of 5 and 15 cmH2O to apply a near-maximal physiologic %⌬A, comparable to that of severe mechanical ventilation, or between 1 and 30 cmH2O, to apply a supraphysiologic %⌬A. We pause ventilation for 20 min and determine T at the meniscus that is present at the flooded alveolar mouth. We determine alveolar air pressure at the trachea, alveolar liquid phase pressure by servo-nulling pressure measurement, and meniscus radius by confocal microscopy, and we calculate T according to the Laplace relation. Over 60 ventilation cycles, application of maximal physiologic %⌬A to alveoli flooded with 4.6% albumin solution does not alter T; supraphysiologic %⌬A raise T, transiently, by 51 Ϯ 4%. In separate experiments, we find that addition of exogenous surfactant to the alveolar liquid can, with two cycles of maximal physiologic %⌬A, reduce T by 29 Ϯ 11% despite the presence of albumin. We interpret that supraphysiologic %⌬A likely collapses the interfacial surfactant monolayer, allowing albumin to raise T. With maximal physiologic %⌬A, the monolayer likely remains intact such that albumin, blocked from the interface, cannot interfere with native or exogenous surfactant activity. alveolar edema; albumin; plasma proteins; surfactant; surface tension IN THE ACUTE RESPIRATORY DISTRESS syndrome (ARDS), high alveolar-capillary barrier permeability results in pulmonary edema.1 The liquid that floods the alveolus contains plasma proteins that can inactivate lung surfactant by adsorbing faster than surfactant and, once present at the interface, blocking further surfactant adsorption (21,45,47,53). Plasma proteins have been shown in vitro to increase surface tension, T, in a dose-dependent fashion (18,41,42,45,53). Elevated surface tension may, in turn, underlie a decrease in lung compliance in ARDS (29) and thus contribute to the need for mechanical ventilation. Intratracheal delivery of exogenous surfactant has been tested in six randomized, controlled clinical trials as a therapy for ARDS, a means of reversing surfactant inactivation, but has failed to reduce mortality (5), which remains Ͼ35% (33).The evidence for increased surface tension in ARDS stems from the reduced surface activity of bronchoalveolar lavage fluid (BALF) from ARDS patients (14,18,19,32,34). This reduced surface activity is principally attri...

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