On the mechanism for enhancement of tumor radiation to hyperbaric oxygen in sodium pentobarbital anesthetized rodents.

Abstract

Pentobarbital anesthesia has been observed to increase markedly the effectiveness of respiration of oxygen at 3 atmospheres of pressure absolute to increase the response of early generation isotransplants of C3H mouse tumors to two-dose irradiation. A possible mechanism of this phenomenon is suppression of oxygen utilization by the pentobarbital and hence increasing mean pO2 and oxygen diffusion lengths. Measurements of QO2 of suspension of MCaIV and FSaII cells from freshly excised tumor tissue have been measured for cells suspended in PBS, Hank's buffered with HEPES +/- glutamate. The oxygen utilization by these tumor cells in vitro (when measured at congruent to 10 minutes after excision) is low, viz. 1 nmole/min/mg protein as compared with 6-9 nmoles/min/mg protein for established cell lines cultured in vitro. The suppression of QO2 by 2mM pentobarbital is less than 10%. This is a concentration of pentobarbital that is judged to be close to that which obtains in the tissues of the animals in the radiation response assays. Pentobarbital at .2mM did not change the cell survival characteristics of Chinese V79 cell spheroids irradiated in vitro. The results of these experiments do not indicate the suppression of oxygen utilization is an important contributor to the observed phenomenon of the increased response of tumors irradiated in mice respiring oxygen at high pressure. The role of hypothermia produced by the anesthesia is under further study.