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Related Experiment Video

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Quantifying Single Microvessel Permeability in Isolated Blood-perfused Rat Lung Preparation

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Published on: June 30, 2014

Phenotypic heterogeneity in lung capillary and extra-alveolar endothelial cells. Increased extra-alveolar endothelial

Kevin Lowe¹, Diego Alvarez, Judy King

¹Center for Lung Biology, University of South Alabama College of Medicine, Mobile, Alabama 36688, USA.

The Journal of Surgical Research

|October 24, 2007

Summary

Increased permeability in lung vessels causes fluid buildup. Different vessel types lead to distinct fluid accumulation sites and varying acute respiratory distress syndrome outcomes, challenging classic edema models.

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Area of Science:

Pulmonary medicine
Vascular biology
Pathophysiology

Background:

Acute respiratory distress syndrome (ARDS) involves increased pulmonary vascular permeability and fluid/protein leakage into lung interstitium.
The traditional model of pulmonary edema formation is challenged by findings of increased extra-alveolar vessel permeability in acute lung injury.
This study investigates whether site-specific endothelial permeability increases (capillary vs. extra-alveolar) cause distinct fluid accumulation and pathophysiology.

Purpose of the Study:

To determine if increased permeability of capillary or extra-alveolar endothelium causes extravascular fluid accumulation.
To ascertain if different pathophysiological outcomes result from site-specific increases in endothelial permeability.

Main Methods:

Isolated lungs were perfused with thapsigargin to increase extra-alveolar endothelial permeability.
Isolated lungs were perfused with 4alpha-phorbol 12, 13-didecanoate to increase capillary endothelial permeability.

Main Results:

Both treatments equally increased whole lung vascular permeability but localized fluid accumulation differently.
Thapsigargin induced fluid cuffing around large vessels, while 4alpha-phorbol 12, 13-didecanoate caused alveolar flooding.
Dynamic lung compliance decreased with large vessel cuffing but not with alveolar flooding.

Conclusions:

Vascular segment-specific permeability increases lead to distinct pathophysiological outcomes in the lungs.
Insults causing ARDS may target either extra-alveolar or capillary vascular segments, resulting in different clinical sequelae.