Modification of photodynamic therapy-induced hypoxia by fluosol-DA (20%) and carbogen breathing in mice.

Modification of photodynamic therapy-induced hypoxia by fluosol-DA (20%) and carbogen breathing in mice.
复制标题

DOI:
--
复制
发表时间:
1988-06
期刊:
影响因子:
11.2
通讯作者:
V. Fingar;Thomas S. Mang;B. W. Henderson
V. Fingar;Thomas S. Mang;B. W. Henderson
中科院分区:
医学1区
文献类型:
--
作者:
V. Fingar;Thomas S. Mang;B. W. Henderson

文献摘要

被引文献

相似文献

研究了光动力治疗(PDT)前全氟化学乳剂和碳(95% O2, 5% CO2)呼吸的管理,以确定肿瘤氧合水平的增加如何影响PDT诱导的肿瘤破坏。携带RIF肿瘤的C3H/HeJ小鼠在治疗前24小时注射5 ~ 10 mg/kg的双血卟啉醚。在肿瘤暴露于135 J/cm2的630 nm光治疗前1小时,动物注射12 ml/kg氟索尔- da(20%),然后进行碳呼吸或12 ml/kg生理盐水和空气呼吸(对照组)。在治疗后立即和不同时间测量肿瘤缺氧部分的变化、肿瘤细胞克隆性降低的时间过程和肿瘤反应。氟索- da(20%)和碳呼吸可延迟pdt所致缺氧的发生,直至治疗后1小时。治疗4 h后观察肿瘤进展性缺氧。肿瘤保持良好氧合的时间与观察到的肿瘤细胞存活率增加相吻合。只有在肿瘤细胞缺氧后,肿瘤细胞的克隆性才会下降。这些发现与PDT前给予氟索- da(20%)和碳呼吸的动物的完全肿瘤反应延迟24小时一致。两组患者在长期肿瘤反应和治愈率方面仅有微小差异。第二个系列的实验是为了评估在高肿瘤光敏剂水平下,辅助使用氟索- da(20%)和碳呼吸与PDT的治疗优势。在注射剂量为50mg /kg的双血卟啉醚时,没有观察到这种优势。氟索- da(20%)和碳呼吸并没有降低pdt诱导的微血管损伤程度,也没有通过光治疗维持高水平的肿瘤氧合,也没有改变治疗后肿瘤细胞的杀伤程度。
The administration of a perfluorochemical emulsion and carbogen (95% O2, 5% CO2) breathing before photodynamic therapy (PDT) was studied to determine how increased levels of tumor oxygenation may affect PDT-induced tumor destruction. C3H/HeJ mice bearing the RIF tumor were given injections of 5 to 10 mg/kg of dihematoporphyrin ethers 24 h prior to treatment. Animals were given injections of 12 ml/kg of Fluosol-DA (20%) followed by carbogen breathing or 12 ml/kg of saline and air breathing (controls) 1 h before tumors were exposed to 135 J/cm2 of 630-nm light treatment. Changes in the hypoxic fraction of tumors, the time course for decreases in tumor cell clonogenicity, and tumor response were measured immediately and at various times after treatment. The administration of Fluosol-DA (20%) and carbogen breathing was found to delay the onset of PDT-induced hypoxia through the first hour posttreatment. Progressive tumor hypoxia was observed after 4 h posttreatment. The time period in which tumors remained well oxygenated coincided with observations of increased tumor cell survival. Decreases in tumor cell clonogenicity were observed only after tumor cells became hypoxic. These findings were consistent with the 24-h delay in complete tumor response in animals given Fluosol-DA (20%) and carbogen breathing before PDT. There were only minor variations in long-term tumor response and cure observed between the two groups tested. A second series of experiments was done to assess any treatment advantage of the adjuvant use of Fluosol-DA (20%) and carbogen breathing with PDT at high tumor photosensitizer levels. At an injected dose of 50 mg/kg of dihematoporphyrin ethers, no such advantage was observed. The administration of Fluosol-DA (20%) and carbogen breathing did not reduce the extent of PDT-induced microvascular damage, maintain high levels of tumor oxygenation through light treatment, or modify the extent of tumor cell kill following treatment.