He D P, Hampton J A, Keck R, Selman S H
Department of Surgery, Medical College of Ohio, Toledo 43699.
Photochem Photobiol. 1991 Nov;54(5):801-4. doi: 10.1111/j.1751-1097.1991.tb02093.x.
Previous studies in our laboratory have demonstrated that photodynamic therapy (PDT) of experimental bladder tumors leads to rapid destruction of the endothelial lining within the tumor microvasculature. Endothelial cell death during PDT may be a consequence of direct cell injury resulting from retention of photosensitizer within the endothelial cell or, alternatively, result from intravascular activation of circulating photosensitizer with subsequent indirect endothelial damage. In the experiments described here, we investigated the possibility that photosensitizer retained within the endothelial cell was sufficient to cause endothelial cell injury in the absence of circulating drug. The experimental model was rat aorta photosensitized in vivo via the intravenous injection of tin(II) etiopurpurin dichloride (SnET2), and subsequent in situ or in vitro (in explant culture) light (670 nm) treatment from an argon pumped dye laser. Damage to the lining of the aorta was assessed morphometrically by determining the areal density of silver stained endothelial cells. Results indicate that purpurin SnET2-PDT directly damages the endothelial lining.
我们实验室之前的研究表明，对实验性膀胱肿瘤进行光动力疗法（PDT）会导致肿瘤微血管内的内皮细胞层迅速遭到破坏。光动力疗法期间内皮细胞死亡可能是由于内皮细胞内保留的光敏剂导致直接细胞损伤的结果，或者是由于循环光敏剂的血管内激活以及随后的间接内皮损伤所致。在本文所述的实验中，我们研究了在没有循环药物的情况下，内皮细胞内保留的光敏剂是否足以引起内皮细胞损伤。实验模型是通过静脉注射二氯化锡（II）乙卟啉（SnET2）在体内使大鼠主动脉光敏化，随后用氩泵浦染料激光进行原位或体外（外植体培养）光照（670nm）处理。通过测定银染内皮细胞的面积密度，用形态计量学方法评估主动脉内膜的损伤情况。结果表明，紫红素SnET2-光动力疗法直接损伤内皮细胞层。
