ABSTRACT
The vascular endothelium now is well recognized as a tissue that acts as an exquisitely responsive sensor to its biochemical and mechanical environment and then transduces
those stimuli to modulate both its own physiology as well as the physiology of the underlying vascular wall (Davies, 1995). Even the classic concept of the endothelium as a nonthrombogenic lining impermeable to macromolecules depends and is modulated by the nature and level of these environmental factors. The “normal”, physiologic endothelium maintains its nonthrombogenic and macromolecule barrier function primarily due to the predominant environment in which it dwells. Thus, the optimal blend of biochemicals in the blood plasma along with an active mechanical environment involving flow, stretch and pressure contributes to a healthy endothelium containing macromolecule impermeable, intercellular tight junctions, which still cannot be completely replicated in cell culture. Furthermore, the arterial endothelium exposed to blood flow-associated shear stress of 15-20 dynes/cm2 is known to dramatically increase its antithrombogenic nature through the synthesis and release of a variety of agents, including nitric oxide (NO) (Uematsu et al., 1995), prostacyclin (PGI2) (Frangos et al., 1985; Grabowski et al., 1985), and the fibinolytic agent, tissue plasminogen activator (t-PA) (Diamond et al., 1989).
