Certain Chemorheologic Considerations Regarding the Blood Vascular Interface with Particular Reference to Coronary Artery Disease

Abstract

The locations of coronary atheroma in a hyperlipemic dog are shown to occur at points in the arterial tree where one would expect the most intense exposure to physical stress. Studies are presented that were designed to quantify certain aspects of the histological and physicochemical response of the arterial intima to a variety of acutely imposed mechanical stresses. These results indicate that the endothelial-cell population has an acute yield stress to shear of about 400 dynes/cm 2 ; that exposure to stress in excess of this is associated with cytological and chemical changes, suggesting that physical processes are occurring, such as "yielding," "melting," "dissolving," "imbibition," and "permeation" of the interfacial tissues; and that even in the absence of cytological changes, the permeability of the interface for albumin is increased by increasing the stress acting on the interface whether in shear, compression, or tension. The relations of these events to tissue rheology, the strain energy density of the interfacial region, and the "critical energy" of molecular separation in the interfacial substance are discussed in terms of the energetics of molecular interactions. Classical rate process theory is used in an effort to express these ideas in more conventional chemical terminology. Arguments are presented in support of the postulate that mechanical energy added to the vascular interface may be used either as the driving force for a chemical process or can be used to increase the rate constant for such processes as interfacial yielding, melting, dissolving, imbibition, or permeation by serum proteins. The added mechanical energy is assumed to increase the rate constant by increasing the number of defects in the array of interfacial molecules or by increasing the average energy level of the molecules, thus decreasing the activation energy for the particular process being considered. As a corollary to this, it follows that the chemical "barrier function" of the vascular interface is enhanced by maintaining its energy density as low as possible and will be degraded in regions of increased energy density. These notions lead to the suggestion that the topography of increased serum protein flux as well as atheromatous plaques is determined among other things by the distribution of mechanically induced increased energy density in the vascular interface.