CRITICAL PO2 IN BRAIN

肿瘤PO2的变化，已知发生在辐射后 [O‘Hara等人，Rad.Res.144：222,1995]可能是由于 肿瘤细胞的肿瘤血流和/或氧气消耗。在这 我们已经确定了10GyX辐射的影响，给出了 活体，基于从两个细胞中获得的细胞的耗氧率 不同的可移植小鼠肿瘤，RIF-1和MTG-B，展示 辐射引起的缺氧和复氧的不同动力学。 将这些数据与未照射的匹配细胞进行比较 肿瘤，以及相同肿瘤类型的细胞也被照射为 体外培养的单层膜。单细胞制剂以10%的比例悬浮 介质中的葡聚糖，以及由EPR线宽决定的O2消耗 中性氮氧化物的测量。用于比较 实验中，实验值表示为 辐照细胞对未辐照对照细胞的耗氧率 同一天。细胞消耗氧气的速率来源于 观察到的最低肿瘤氧分压时的照射肿瘤(6小时 对于MTG-B，RIF-1的24小时)大约是 未照射的对照组。培养的MTG-B细胞表现为一过性 照射后2-6小时氧气消耗增加，而24小时 照射后，这一比率低于未照射的细胞 (P&lt；0.05，n=4)。这些结果支持这样的假设： 照射后肿瘤PO2的变化可以至少部分地导致， 从辐射引起的肿瘤细胞耗氧量的变化。

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.