Abstract

Vascular damage and blood flow stasis are consequences of photodynamic therapy (PDT) of solid tumors using many photosensitizers. Microvascular stasis and resulting hypoxia are effective means to produce cytotoxicity and tumor regression. The observation of blood flow stasis after photodynamic therapy results from a combination of damage to sensitive sites within the microvasculature and the resulting physiological responses to this damage. A generalized hypothesis for the mechanisms leading to vessel stasis begins with perturbation and damage to endothelial cells during light treatment of photosensitized tissues. Endothelial cell damage leads to the establishment of thrombogenic sites within the vessel lumen and this initiates a physiological cascade of responses including platelet aggregation, the release of vasoactive molecules, leukocyte adhesion, increases in vascular permeability, and vessel constriction. These effects from damage combine to produce blood flow stasis.

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