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Updated: May 16, 2026
In vivo Measurement of the Mouse Pulmonary Endothelial Surface Layer
Published on: February 22, 2013
[Change of adhesion molecules in the lungs of rat with decompression sickness]
Xiao-Chen Bao1, Yi-Qun Fang, Jun Ma
1Naval Medical Research Institute, Shanghai 200433, China.
Objective:
To investigate the change of adhesion molecules in the lungs of rats suffered with decompression sickness (DCS).
Methods:
Male SD rats were placed in the hyperbaric chamber, the chamber was compressed within 3 minutes to depths of 7 absolute atmosphere (ATA) and held at the designated depth for 60 min, then rapidly decompressed (3 min) to the surface. Rats were observed for signs of DCS after decompression. The brains, hepatis, and lungs were removed at 30 min, 6 h, 24 h post decompression, fixed and stained with hematoxylin eosin for routine histologic analysis. Lung paraffin sections were immunostained for the expression of intercellular adhesion molecule-1 (ICAM-1), E-selectin and major histocompatibility complex class II molecule (MHC-II). 2% evans blue dye in normal saline was injected 30 minutes prior to 6 h, 24 h before decompression. After 30 min, animals were perfused with 0.9% normal saline and lungs were harvested. Evans blue in the plasma was quantified by wavelength spectrophotometric analysis at 620 nm.
Results:
Results showed that there were hemorrhage and edema changes in the lungs, liver and brain at 30 min post decompression. Compared with control animals maintained at 1 ATA, the levels of E-selectin, ICAM-1 and MHC-II in the lungs of DCS rats were significantly increased post decompression. Compared with control animals, evans blue in the plasma was much higher at 6 h, 24 h post decompression.
Conclusion:
The bubble-induced adhesion molecule-mediated endothelial activation may be involved in the pathogenesis of DCS.
