Acute Vascular Endothelial Changes Associated with Increased Blood Velocity Gradients
The purpose of this study is to quantify the acute changes in endothelial histology that are associated with an induced increase in blood velocity. A nontraumatic intra-aortic device was designed to produce a rapid convergence of the aortic blood stream into a narrow channel along the ventral aspect of the thoracic aorta in dogs. The endothelial surface overlying this channel was exposed to a broad range of surface shearing stress by the accelerated blood flow. Techniques were developed to quantify the resulting distribution of shearing stress so that the stress to which the endothelial surface was exposed at every point along the channel could be determined. Special histologic techniques were developed using formalin fixation and gelatin embedding of the tissue so that endothelial cytology could be studied and criteria for normal cells established. Using these criteria, cell counts were done to establish the "normal" endothelial cell population density as a function of stress exposure. The stress corresponding to the mode of these cell density distribution curves was defined as the acute yield stress (τc). The acute yield stress for endothelial cells was found to be 379±85 (SD) dynes/cm2. Exposure to stress in excess of this value for periods as short as one hour resulted in marked deterioration of the endothelial surface consisting of endothelial cytoplasmic swelling, cell deformation, cell disintegration, and finally dissolution and erosion of cell substance. The relationship of these events to cellular rheology and interfacial chemistry is discussed.
- endothelial rheology
- yield stress
- endothelial injury
- vessel wall shearing stress
- vascular fluid mechanics
- blood-endothelial interfacial chemistry
- thoracic aorta
- Accepted November 21, 1967.
- © 1968 American Heart Association, Inc.