Brain and cerebrospinal oxygen tensions have been measured in rats breathing air or in various high pressures of oxygen (OHP). Addition of 5% CO2 to the inspired oxygen raised cerebral oxygen tensions when rats were exposed to 2 atm abs or above. Inhibition of 75% hemoglobin saturation by para-aminopropriophenone lowered cerebral pO2 in rats breathing air, but not in rats exposed to OHP. The rate of rise of cerebral pO2 to a steady level after rapid compression was found to be faster than the rate of fall to a steady level following decompression. Addition of CO2 to the inspired gas mixture increased the rate of rise of cerebral pO2. The anesthetics urethane and pentobarbital sodium did not affect cerebral pO2 in rats breathing air or oxygen at 4 atm. The results are discussed in relation to factors contributing to oxygen poisoning at high pressures. Submitted on October 30, 1962
Single cell suspensions of two allogeneic tumours (W-256 and Y-P388) injected intravenously produced macrocolonies in the lungs of rats. Colony forming efficiency (CFE, the number of colonies produced by each viable cell injected) was low in 6-week or older rats but was markedly increased by 1000-1500 rad local thoracic irradiation (LTI) given 7-14 days before the tumour cell injection, or by antilymphocytic serum (ALS) but not by sublethal whole body irradiation (WBI). Similarly, LTI increased the incidence of pulmonary metastases produced by a solid tumour growing in the leg muscle. Stimulation of CFE by LTI was a strictly local phenomenon and not due to effects of irradiation on thymus, spleen or other tissues of the rat. LTI failed to increase CFE in immunized rats. It is concluded that (1) LTI stimulates clonogenic growth of tumour cells arrested in the lungs, by causing inflammatory reactions accompanied by regenerative cellular proliferation of lung tissue, which increases the “plating” efficiency of tumour cells, (2) the increase in CFE in lungs is not due to suppression of immunity to tumour growth by LTI.
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Fig. 3
Summary.-Two rapidly growing allogeneic tumours, sublines of Yoshida (Y-P388) and Walker (W-256) injected intravenously in single cell suspensions produced tumour macrocolonies in the lungs of rats within 7 days. Y-P388 produced similar but fewer colonies in the kidneys. Colony forming efficiency (CFE) in lung was high in weanling rats given either sublethal whole body irradiation (WBI) or a single dose of rabbit anti-rat lymphocytic serum (ALS) to suppress immunity. In immunologically intact weanlings CFE was much lower and many 7-day old colonies showed signs of regression. CFE for primary tumour cell challenges decreased rapidly and markedly with increase in age of host during the first 1-2 weeks after weaning. This resistance to growth of a primary challenge in lungs of older rats was not significantly reduced by WBI but was decreased by ALS. CFE of a secondary challenge of tumour cells injected intravenously in rats which had been previously immunized with heavily irradiated (HR) tumour cells was very low; it was not significantly increased by WBI but was moderately increased by ALS. In weanling rats given lethal (900 ra4) WBI, 1 hour before intravenous injection of tumour cells, treatment with bone marrow (BM) cells derived from normal adult donors increased CFE, whereas BM (or spleen) cells from immunized donors decreased CFE. The results suggest that ALS and WBI not only increase tumour CFE by suppressing immunity to tumour growth but also " condition " host tissue (tumour bed) in such a way as to facilitate the survival, " take " and initial replication of grafted tumour cells before the rats recover from the immunosuppressive effects of these treatments.
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