Fingar V H
Department of Surgery, James Graham Brown Cancer Center, University of Louisville, Kentucky 40292, USA.
J Clin Laser Med Surg. 1996 Oct;14(5):323-8. doi: 10.1089/clm.1996.14.323.
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.
使用多种光敏剂对实体瘤进行光动力疗法（PDT）会导致血管损伤和血流淤滞。微血管淤滞以及由此产生的缺氧是产生细胞毒性和肿瘤消退的有效手段。光动力疗法后观察到的血流淤滞是由于微血管内敏感部位受损以及对这种损伤产生的生理反应共同作用的结果。导致血管淤滞机制的一个普遍假设始于对光敏化组织进行光照处理期间内皮细胞受到的扰动和损伤。内皮细胞损伤导致血管腔内形成血栓形成部位，这引发了一系列生理反应，包括血小板聚集、血管活性分子的释放、白细胞黏附、血管通透性增加和血管收缩。这些损伤效应共同作用导致血流淤滞。
