Tumor PO2 changes during photodynamic therapy depend upon photosensitizer type and time after injection
Tumor PO2 changes during photodynamic therapy depend upon photosensitizer type and time after injection
复制标题
DOI：
10.1016/s1095-6433(01)00545-1
复制
发表时间：
2002-05-01
影响因子：
2.3
通讯作者：
Swartz, H
中科院分区：
文献类型：
--
作者：
Pogue, BW;O'Hara, JA;Swartz, H
在这项研究中，血管和组织的氧变化引起的光动力疗法在RIF-1肿瘤进行了检查，使用电子顺磁共振（EPR）血氧饱和度。两种光敏剂，包括维替泊芬（脂质制剂中的BPD-MA）和氨基乙酰丙酸诱导的原卟啉IX（ALA-PPIX）。的光照射，足以诱导亚治愈性损伤的肿瘤组织，并在Po-2和血管灌注的瞬态变化进行了研究。当用基于ALA-PPIX的光动力疗法治疗时，观察到组织氧合的大幅增加（从3至9.5 mmHg），其在治疗期间持续，并且在治疗后48小时恢复到基线水平的少量残余增加。使用基于维替泊芬的光动力疗法，一组动物在注射后15分钟照射，并且相对于照射前水平表现出氧合的小幅降低。第二组在注射后3小时进行照射，并在治疗结束时表现出平均Po-2（从3到15 mmHg）的大幅增加。这些观察结果表明，在某些治疗条件下，光动力疗法显著增加组织Po-2，其潜在原因是由于细胞损伤导致的局部血流增加或局部氧代谢消耗减少。(C)2002年爱思唯尔科技有限公司All rights reserved.
In this study, the vascular and tissue oxygen changes induced by photodynamic therapy in the RIF-1 tumor were examined, using electron paramagnetic resonance (EPR) oximetry. Two photosensitizers, including verteporfin (BPD-MA in a lipid-based formulation) and aminolevulinic acid-induced protoporphyrin IX (ALA-PPIX). were investigated with optical irradiation, sufficient to induce sub-curative damage in the tumor tissue, and the transient changes in Po-2 and vascular perfusion were examined. A large increase in tissue oxygenation (from 3 up to 9.5 mmHg) was observed when treated with ALA-PPIX based photodynamic therapy, which lasted during the treatment and a small residual increase that returned back to baseline levels by 48 h after treatment. With verteporfin-based photodynamic therapy, one group of animals was irradiated 15 min after injection and exhibited a small decrease in oxygenation relative to preirradiation levels. The second group was irradiated at 3 h after injection and exhibited a large increase in the average Po-2 (from 3 to 15 mmHg) by the end of the treatment. These observations indicate that photodynamic therapy significantly increases tissue Po-2 under certain treatment conditions, with the potential cause being either increased local blood flow or decreased local oxygen metabolic consumption due to cellular damage. (C) 2002 Elsevier Science Inc. All rights reserved.