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1 Department of Experimental Medicine, University of Milano-Bicocca, 20052 Monza; and 2 Department of Animal Biology, University of Pavia, 27100 Pavia, Italy
Mild pulmonary interstitial edema
was shown to cause fragmentation of interstitial matrix proteoglycans.
We therefore studied compartmental fluid accumulation by light and
electron microscopy on lungs of anesthetized rabbits fixed in situ by
vascular perfusion after 0.5 ml · kg
1 · min
1 iv saline
infusion for 180 min causing ~6% increase in lung weight. Morphometry showed that a relevant portion (44%) of extravascular fluid is detected early in the alveolar septa, 85% of this fluid accumulating in the thick portion of the air-blood barrier. The arithmetic mean thickness of the barrier increased in interstitial edema from 1.06 ± 0.05 (SE) to 1.33 ± 0.06 µm. The
harmonic mean thickness increased from 0.6 ± 0.03 to 0.86 ± 0.07 µm, mostly due to thickening of the thin portion causing an
increase in gas diffusion resistance. Despite some structural damage,
the air-blood barrier displays a relatively high structural resistance
providing a safety factor against the development of severe edema. It
is suggested that the increase in extra-alveolar perivascular space occurs as a consequence of fluid accumulation in the air-blood barrier.
thin and thick portions of the air-blood barrier; extracellular matrix; fibrillar collagen; basement membranes; gas diffusion; fluid accumulation; proteoglycans; top and bottom lung regions
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