Summary of Workshop 3a: Hemodynamic Injury

  • Donald L. Fry
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 104)


The workshop began with five-minute presentations from each of the participants who were asked to give a brief panoramic view of the present state of knowledge regarding intravascular fluid mechanics as a factor in thromboatherogenesis. This served as a review for those in related fields and as a point of departure for subsequent discussion. Dr. Nerem began with a review of basic fluid mechanics. Hemodynamic stress was defined and shown to be resolved into two components: a pressure and a shear stress. Types of flow fields that can occur in a variety of conduit geometries were also reviewed (1). The extraordinary complexities that can occur in these fields were emphasized. Although flow tends to be streamlined in the vascular system, a branching conduit such as the arterial tree can manifest significant variation of shear stress from point to point and is particularly vulnerable to localized areas of disturbed flow patterns and flow separation. It was noted that the maintenance of a stable flow pattern in any conduit configuration depends on subtle geometric considerations and that, given a stable flow conduit system, subtle distortions of this geometry will destroy its streamlined properties. For example, the overdistended and distorted arterial tree associated with hypertension might be particularly predisposed to unstable flow patterns. The endothelial surface was found to be sensitive to adjacent hemodynamic events. Endothelial permeability was shown to increase monotonically with acute exposure to increasing levels of shear stress.


Flow Separation Arterial Tree Evans Blue Endothelial Permeability Endothelial Surface 
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  1. 1.
    Nerem, R.M., Rumberger, J.A., Jr., Gross, D.R., Muir, W.W., and Geiger, G.L. (1976) J. Cardiovasc. Res. 10 (3), 301–313.CrossRefGoogle Scholar
  2. 2.
    Chien, S. (1976) Ann. N.Y. Acad. Sci. 275, 10–27.PubMedCrossRefGoogle Scholar
  3. 3.
    Forstrom, R.J., Bartelt, K., Blackshear, P.L., and Wood, T. (1975) Trans. Am. Soc. Artif. Int. Organs 21, 602–607.Google Scholar
  4. 4.
    Murphy, E.A., Rowsell, H.C., Downie, H.G., Robinson, G.A., and Mustard, J.F. (1962) Can. Med. Assoc. J. 87, 259–274.PubMedGoogle Scholar
  5. 5.
    Fry, D.L. (1976) Cerebrovascular Diseases (Scheinberg, P., Ed.), Raven, New York, pp. 77–95.Google Scholar

Copyright information

© Plenum Press, New York 1978

Authors and Affiliations

  • Donald L. Fry
    • 1
  1. 1.Laboratory of Experimental AtherosclerosisNational Heart, Lung, and Blood InstituteBethesdaUSA

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