Reduced surface tension normalizes static lung mechanics in a rodent chronic heart failure model.

Abstract

Chronic elevation of pulmonary microvascular pressure in chronic heart failure results in compensatory changes in the lung that reduce alveolar fluid filtration and protect against pulmonary microvascular rupture. To determine whether these compensatory responses may have maladaptive effects on lung function. Six weeks after myocardial infarction (chronic heart failure model) rat lung composition, both gross and histologic; air and saline mechanics; surfactant production; and immunological mediators were examined. An increase in dry lung weight, due to increased insoluble protein, lipid and cellular infiltrate, without pulmonary edema was found. Despite this, both forced impedance and air pressure-volume mechanics were normal. However, there was increased tissue stiffness in the absence of surface tension (saline pressure-volume curve) with a concurrent increase in both surfactant content and alveolar type II cell numbers, suggesting a novel homeostatic phenomenon. These studies suggest a compensatory reduction in pulmonary surface tension that attenuates the effect of lung parenchymal remodeling on lung mechanics, hence work of breathing.