Cigarette smoke extract increases albumin flux across pulmonary endothelium in vitro
Cigarette smoking causes lung inflammation, and a characteristic of inflammation is an increase in vascular permeability. To determine if cigarette smoke could alter endothelial permeability, we studied flux of radiolabeled albumin across monolayers of porcine pulmonary artery endothelium grown in culture on microporous membranes. Extracts (in either dimethylsulfoxide or phosphate-buffered saline) of cigarette smoke in a range estimate of concentrations simulating cigarette smoke exposure to the lungs in vivo caused a dose-dependent increase in albumin flux that was dependent on extracellular divalent cations and associated with polymerization of cellular actin. The effect was reversible, independent of the surface of endothelial cells exposed (either luminal or abluminal), and due primarily to components of the vapor phase of smoke. The effects occurred without evidence of cell damage, but subtle morphological changes were produced by exposure to the smoke extracts. These findings suggest that cigarette smoke can alter permeability of the lung endothelium through effects on cytoskeletal elements.
- Research Organization:
- Portland Veterans Administration Medical Center, OR (USA)
- OSTI ID:
- 6276982
- Journal Information:
- J. Appl. Physiol.; (United States), Vol. 66:1
- Country of Publication:
- United States
- Language:
- English
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Related Subjects
ALBUMINS
MEMBRANE TRANSPORT
CELL MEMBRANES
PERMEABILITY
LUNGS
INFLAMMATION
TOBACCO SMOKES
BIOLOGICAL EFFECTS
CALCIUM
DOSE-RESPONSE RELATIONSHIPS
ENDOTHELIUM
MAGNESIUM
SWINE
AEROSOLS
ALKALINE EARTH METALS
ANIMAL TISSUES
ANIMALS
BODY
CELL CONSTITUENTS
COLLOIDS
DISPERSIONS
DOMESTIC ANIMALS
ELEMENTS
MAMMALS
MEMBRANES
METALS
ORGANIC COMPOUNDS
ORGANS
PATHOLOGICAL CHANGES
PROTEINS
RESIDUES
RESPIRATORY SYSTEM
SMOKES
SOLS
SYMPTOMS
TISSUES
VERTEBRATES
550901* - Pathology- Tracer Techniques