The core pathology is disruption of the capillary-endothelial interface: this actually refers to two separate barriers the endothelium and the basement membrane of the alveolus.
The pathophysiology of unstable angina is the reduction of coronary flow due to transient platelet aggregation on apparently normal endothelium, coronary artery spasms, or coronary thrombosis.
Due to infection, fish have produced lesions in the vascular endothelium that cause blood extravasation, leading to hemorrhages and petechias at the surface of internal organs.
Exposure to second-hand smoke from environmental exposure has also been shown to promote changes in blood vessel lining (endothelium) which is a precursor to atherosclerosis.
The antithrombotic effect of dextran is mediated through its binding of erythrocytes, platelets, and vascular endothelium, increasing their electronegativity and thus reducing erythrocyte aggregation and platelet adhesiveness.