CRITICAL PO2 IN BRAIN

已知在照射后发生的肿瘤pO 2的变化 [O 'Hara等人，Rad.Res.144：222，1995]可能是由于 肿瘤灌注和/或肿瘤细胞的氧消耗。 在这 研究中，我们确定了10戈伊X射线照射的效果， 在体内，根据从两个组织中收获的细胞的氧消耗速率， 不同的可移植小鼠肿瘤，RIF-1和MTG-B， 辐射诱导的缺氧和复氧的不同动力学。 将这些数据与来自未照射细胞的匹配细胞进行比较。 肿瘤，并且还与相同肿瘤类型的细胞一起照射， 体外单层。 将单细胞制剂悬浮于10% 右旋糖酐在培养基中，和O2消耗由EPR线宽确定 中性氮氧化物的测量。 之间的比较 在实验中，实验值表示为 辐照细胞对未辐照对照的O2消耗率 于同日起 细胞消耗O2的速率来自于 在观察到的最低肿瘤pO 2时（6小时）照射的肿瘤 对于MTG-B，对于RIF-1为24小时）约为 未辐照对照。 培养的MTG-B细胞表现出短暂的 照射后2-6小时增加O2消耗，而24小时 照射后，该速率低于未照射的细胞 （p<0.05，n=4）。 这些结果支持了以下假设： 照射后肿瘤pO 2的变化，至少部分地， 来自辐射引起的肿瘤细胞耗氧变化。

The changes in tumor pO2, known to occur after irradiation [O'Hara, et al., Rad.Res.144:222, 1995] may result from alterations of tumor perfusion and/or oxygen consumption by the tumor cells. In this study we have determined the effects of 10 Gy X-irradiation, given in vivo, upon the rates of oxygen consumption of cells harvested from two different transplantable murine tumors, RIF-1 and MTG-B, that exhibit different kinetics of radiation-induced hypoxia and reoxygenation. These data were compared with matched cells from non-irradiated tumors, and also with cells of the same tumor type irradiated as monolayers in vitro. Single cell preparations are suspended in 10% dextran in medium, and O2 consumption determined by the EPR linewidth measurement of a neutral nitroxide. For comparison between experiments, the experimental values are expressed as a ratio of the rate of O2 consumption by irradiated cells to unirradiated controls on the same day. The rate of O2 consumption by cells derived from irradiated tumors at the time of the lowest observed tumor pO2 (6 hr for MTG-B, 24 hr for RIF-1) was approximately twice that of unirradiated controls. Cultured MTG-B cells showed transient increased O2 consumption 2-6 hr post-irradiation, while 24 hr post-irradiation this rate was less than that of unirradiated cells (p<.05, n=4). These results support the hypothesis that post-irradiation changes in tumor pO2 can result, at least in part, from radiation-induced changes in oxygen consumption by tumor cells.