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Published ahead of print on April 16, 2009, doi:10.1164/rccm.200809-1506OC

Am. J. Respir. Crit. Care Med., Volume 180, Number 2, July 2009, 181-187

A more recent version of this article appeared on July 15, 2009
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Submitted on September 26, 2008
Accepted on April 15, 2009

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

Dani-Louise Dixon1*, Carmine G De Pasquale2, Hilde R De Smet3, Sonja Klebe4, Sandra Orgeig5, and Andrew D Bersten1

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

* To whom correspondence should be addressed. E-mail: dani.bryan{at}flinders.edu.au.

Rationale: Chronic elevation of pulmonary microvascular pressure in chronic heart failure results in compensatory changes in the lung which reduce alveolar fluid filtration and protect against pulmonary microvascular rupture. Objective: To determine whether these compensatory responses may have maladaptive effects on lung function. Methods: Six weeks following myocardial infarction (chronic heart failure model) rat lung composition, both gross and histological, 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. Conclusion: 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






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