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1 Department of Anesthesiology and Cardiovascular-Pulmonary Research Laboratory, University of Colorado Health Sciences Center, Denver, Colorado 80262; and Departments of 2 Pathology and 3 Pharmacology, College of Medicine, University of South Alabama, Mobile, Alabama 36688
An intact
endothelial cell barrier maintains normal gas exchange in the lung, and
inflammatory conditions result in barrier disruption that produces
life-threatening hypoxemia. Activation of store-operated
Ca2+ (SOC) entry increases the
capillary filtration coefficient
(Kf,c) in the
isolated rat lung; however, activation of SOC entry does not promote
permeability in cultured rat pulmonary microvascular endothelial cells.
Therefore, current studies tested whether activation of SOC entry
increases macro- and/or microvascular permeability in the
intact rat lung circulation. Activation of SOC entry by the
administration of thapsigargin induced perivascular edema in pre- and
postcapillary vessels, with apparent sparing of the microcirculation as
evaluated by light microscopy. Scanning and transmission electron
microscopy revealed that the leak was due to gaps in vessels 
100 µm, consistent with the idea that activation of SOC entry influences
macrovascular but not microvascular endothelial cell shape. In
contrast, ischemia and reperfusion induced microvascular endothelial cell disruption independent of
Ca2+ entry, which similarly
increased Kf,c.
These data suggest that 1)
activation of SOC entry is sufficient to promote macrovascular barrier
disruption and 2) unique mechanisms
regulate pulmonary micro- and macrovascular endothelial barrier functions.
lung; thapsigargin; pulmonary edema; signal transduction; reperfusion injury
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