J Appl Physiol 117: 423–424, 2014;
doi:10.1152/japplphysiol.00631.2014.
Invited Editorial
Invited editorial on “Surface tension in situ in flooded alveolus unaltered by
albumin”
Donald P. Gaver
Department of Biomedical Engineering, Tulane University, New Orleans, Louisiana
Submitted 16 July 2014; accepted in final form 16 July 2014
Address for reprint requests and other correspondence: D. P. Gaver, Dept. of
Biomedical Engineering, Tulane Univ., New Orleans, LA 70118 (e-mail:
[email protected]).
http://www.jappl.org
reported measurements representative of values further from
the pleura where strain rates may deviate from those at the
periphery of the lung? Furthermore, interfacial flows in newly recruited airways and alveoli have undergone large rates
of strain, possibly even greater than the “supraphysiological”
states described in the article of Kharge et al. (5). Dynamic
surfactant transport processes are likely to dominate in these
situations (6), and the present article suggests that surface
tensions should therefore increase transiently during recruitment. The transient duration could be important in determining
optimal ventilation waveforms used to recruit airways, since
maintaining low surface tensions could reduce atelectrauma, a
putative contributor to ventilator-induced lung injury (4).
The study of Kharge et al. (5) contributes significantly to the
literature on surfactant physicochemical interactions and their
relevance to pulmonary mechanics. Most significantly, this
article incorporates substantial bioengineering techniques to
understand the micromechanics of the lung by integrating
high-quality imaging techniques and pressure measurements to
elucidate mechanical properties that are important in pathophysiological conditions. Quantitative information gleaned
from these types of sophisticated studies could provide the data
necessary to develop advanced computational models of the
lung that would link multiple length and time scales. Tools
based on simulations could one day be used by clinicians for
the rational determination of modes of ventilation that could
reduce VALI and improve the outcome for patients with
ARDS, just as they have made an impact in the treatment of
cardiovascular disease (11, 12).
DISCLOSURES
No conflicts of interest, financial or otherwise, are declared by the author(s).
AUTHOR CONTRIBUTIONS
Author contributions: D.P.G. drafted manuscript; D.P.G. edited and revised
manuscript; D.P.G. approved final version of manuscript.
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syndrome (ARDS) is a disorder
that significantly impacts approximately 200,000 individuals
annually in the US and has an associated mortality rate of over
30%. The etiology of ARDS is complex but is frequently
caused by sepsis, aspiration, or smoke inhalation. In vitro
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In a new study published in this issue of the Journal of
Applied Physiology, Kharge et al. (5) use an isolated rat lung
preparation to examine the proposition that vascular proteins
influence lung mechanics. Alveoli were flooded with either
normal saline, blood plasma, 4.6% albumin, high concentrations of albumin, or dextran. The interfacial pressure drop was
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While these measurements determine the surface tension indirectly, they conceptually follow the methods used by wellregarded captive bubble and pulsating bubble techniques (3, 8).
Interestingly, under near-maximal physiologic surface-area
expansion/compression (%⌬A), the introduction of 4.6% albumin did not alter the surface tension in flooded alveoli. In
contrast, only supraphysiological %⌬A raised the surface tension but only transiently. These results are surprising because
they indicate that the compliance of edematous lung units
might not be reduced due to surfactant inactivation during
normal ventilation, as had been assumed from theories of
interfacial sorption and in vitro experiments. These results
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previously thought. Nevertheless, liquid flooding does alter
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lung” phenomenon.
Kharge et al. (5) bring up a number of important followup
questions. It is unclear why the values of surface tension in the
present study are significantly smaller than those measured by
other investigators (9, 10). Since measurements were completed 20 min postventilation, are they equivalent to static
measurements? If so, why are the surface tensions in the
present study below accepted equilibrium values? Perhaps
surfactant release is induced by the local strain (1)? Are the
ACUTE RESPIRATORY DISTRESS
Invited Editorial
424
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