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Reduced Surface Tension Normalizes Static Lung Mechanics in a Rodent Chronic Heart Failure Model

¹ Intensive and Critical Care Unit, Flinders Medical Centre; ² Department of Critical Care Medicine, Flinders University; ³ Cardiac Services, Flinders Medical Centre; ⁴ Department of Medicine, Flinders University; ⁵ Anatomical Pathology, Flinders Medical Centre; ⁶ Department of Pathology, Flinders University; and ⁷ Sansom Institute, School of Pharmacy and Medical Sciences, University of South Australia, Adelaide, Australia

Correspondence and requests for reprints should be addressed to Dani-Louise Dixon, Ph.D., Intensive and Critical Care Unit, Flinders Medical Centre, Bedford Park, Adelaide, South Australia 5042, Australia. E-mail: dani.dixon{at}flinders.edu.au

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.

Key Words: surfactant • alveolar type II cells • pulmonary microvascular pressure • lung morphology

AT A GLANCE COMMENTARY Scientific Knowledge on the Subject Persisting elevation of pulmonary microvascular pressure in chronic heart failure leads to pulmonary remodeling and reduced diffusion coefficient for carbon monoxide. Although this remodeling appears to protect against pulmonary edema, other effects could be harmful. What This Study Adds to the Field Despite increased dry lung weight and stiffer lung tissue, mechanics are normal in a model of chronic heart failure. This paradox is due to a homeostatic response in which surface tension is reduced below normal with a concurrent increase in surface active surfactant content.