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

Abstract

RATIONALE: 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. OBJECTIVES: To determine whether these compensatory responses may have maladaptive effects on lung function. METHODS: 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. MEASUREMENTS AND MAIN RESULTS: 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. CONCLUSIONS: 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.