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Proceedings Paper

Mechanisms of vessel damage in photodynamic therapy (Invited Paper)
Author(s): Victor H. Fingar; Thomas Jeffery Wieman
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Paper Abstract

Vessel constriction and platelet aggregation are observed within the first minutes of light exposure to photosensitized tissues and lead to blood flow stasis, tissue hypoxia, and nutrient depravation. The mechanism for these vessel changes remains unknown, although the release of eicosanoids is implicated. We propose the following hypothesis: Photodynamic therapy results in specific perturbations of endothelial cells which results in a combination of membrane damage, mitochondrial damage, and rearrangement of cytoskeletal proteins. This results in cellular stress which leads to interruption of tight junctions along the endothelium and cell rounding. Cell rounding exposes the basement membrane proteins causing activation of platelets and leukocytes. Activated platelets and leukocytes release thromboxane and other eicosanoids. These eicosanoids induce vasoconstriction, platelet aggregation, increases in vessel permeability, and blood flow stasis.

Paper Details

Date Published: 1 June 1992
PDF: 6 pages
Proc. SPIE 1645, Optical Methods for Tumor Treatment and Detection: Mechanisms and Techniques in Photodynamic Therapy, (1 June 1992); doi: 10.1117/12.60932
Show Author Affiliations
Victor H. Fingar, Univ. of Louisville (United States)
Thomas Jeffery Wieman, Univ. of Louisville (United States)


Published in SPIE Proceedings Vol. 1645:
Optical Methods for Tumor Treatment and Detection: Mechanisms and Techniques in Photodynamic Therapy
Thomas J. Dougherty, Editor(s)

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