Thews Oliver, Vaupel Peter
Institute of Physiology, University of Halle, Magdeburger Str. 6, 06112, Halle (Saale), Germany.
Department of Radiooncology and Radiotherapy, Tumor Pathophysiology Section, University Medical Center Mainz, 55131, Mainz, Germany.
Strahlenther Onkol. 2016 Mar;192(3):174-81. doi: 10.1007/s00066-015-0916-1. Epub 2015 Oct 26.
Inspiratory hyperoxia under hyperbaric conditions has been shown to effectively reduce tumor hypoxia and to improve radiosensitivity. However, applying irradiation (RT) under hyperbaric conditions is technically difficult in the clinical setting since RT after decompression may be effective only if tumor pO2 remains elevated for a certain period of time. The aim of the present study was to analyze the time course of tumor oxygenation and perfusion during and after hyperbaric hyperoxia.
Tumor oxygenation, red blood cell (RBC) flux for perfusion monitoring, and vascular resistance were assessed continuously in experimental rat DS-sarcomas by polarographic catheter electrodes and laser Doppler flowmetry at 1 and 2 atm (bar) of environmental pressure during breathing of pure O2 or carbogen (95 % O2 + 5 % CO2).
During room air breathing, the tumor pO2 followed very rapidly within a few minutes the change of the ambient pressure during compression or decompression. With O2 breathing under hyperbaric conditions, the tumor pO2 increased more than expected based on the rise of the environmental pressure, although the time course was comparably rapid. Breathing carbogen, the tumor pO2 followed with a slight delay of the pressure change, and within 10 min after decompression the baseline values were reached again. RBC flux increased during carbogen breathing but remained almost constant with pure O2, indicating a vasodilation (decrease in vascular resistance) with carbogen but a vasoconstriction (increase in vascular resistance) with O2 during hyperbaric conditions.
Since the tumor pO2 directly followed the environmental pressure, teletherapy after hyperbaric conditions does not seem to be promising as the pO2 reaches baseline values again within 5-10 min after decompression.
高压条件下的吸入性高氧已被证明可有效降低肿瘤缺氧并提高放射敏感性。然而，在临床环境中，在高压条件下进行放射治疗（RT）在技术上具有挑战性，因为减压后的RT可能仅在肿瘤pO2保持升高一段时间才有效。本研究的目的是分析高压高氧期间及之后肿瘤氧合和灌注的时间进程。
通过极谱导管电极和激光多普勒血流仪，在1和2个大气压（bar）的环境压力下，于实验大鼠DS-肉瘤中连续评估肿瘤氧合、用于灌注监测的红细胞（RBC）通量以及血管阻力，实验过程中大鼠呼吸纯氧或卡波金（95% O2 + 5% CO2）。
在呼吸室内空气时，肿瘤pO2在几分钟内就非常迅速地跟随压缩或减压过程中环境压力的变化。在高压条件下呼吸氧气时，尽管时间进程相对较快，但肿瘤pO2的升高幅度超过了基于环境压力升高所预期的幅度。呼吸卡波金时，肿瘤pO2对压力变化的跟随稍有延迟，减压后10分钟内再次达到基线值。卡波金呼吸期间RBC通量增加，但纯氧呼吸时几乎保持恒定，这表明高压条件下卡波金会引起血管舒张（血管阻力降低），而氧气会引起血管收缩（血管阻力增加）。
由于肿瘤pO2直接跟随环境压力变化，高压条件后的远距离治疗似乎前景不佳，因为减压后5 - 10分钟内pO2就会再次达到基线值。
