[The time lapse of the cytostatic effect of ifosfamide].
The time lapse of the effect of ifosfamid on the solid DS carcinosarcoma has been studied using 204 Wistar rats. The main results and the conclusions are as follows: 1. The transplantability of the tumor is abolished two hours after the i.v. application of 180 mg/kg isofamid (cessation of tumor cell proliferation). 2. Yet, the tumor tissue to be grafted is not damaged thoroughly by this treatment. It is possible that the still viable tumor cells were killed by the non-suppressed immune system of the recipients. 3. As determined by trypan blue dye exclusion and registration of glycolytic activity, the main part of tumor cells remains viable. As lately as 4 days after the therapy 80% of the cells incorporate trypan blue and the glycolytic activity is inhibited in the order of 80%. 4. It is to be expected that within two hours, a period sufficient for proliferation inhibition of tumor cells, only 30% of the active form of the drug administered can be found in the tumor. In this context the toxification (activation) kinetics of ifosfamid is discussed and an optimized, programmed infusion is considered. 5. The treatment with ifosfamid does not affect at least up to the third day the tumor hyperacidification attainable by a long-lasting glucose infusion.
[The time lapse of the cytostatic effect of ifosfamide]. The time lapse of the effect of ifosfamid on the solid DS carcinosarcoma has been studied using 204 Wistar rats. The main results and the conclusions are as follows: 1. The transplantability of the tumor is abolished two hours after the i.v. application of 180 mg/kg isofamid (cessation of tumor cell proliferation). 2. Yet, the tumor tissue to be grafted is not damaged thoroughly by this treatment. It is possible that the still viable tumor cells were killed by the non-suppressed immune system of the recipients. 3. As determined by trypan blue dye exclusion and registration of glycolytic activity, the main part of tumor cells remains viable. As lately as 4 days after the therapy 80% of the cells incorporate trypan blue and the glycolytic activity is inhibited in the order of 80%. 4. It is to be expected that within two hours, a period sufficient for proliferation inhibition of tumor cells, only 30% of the active form of the drug administered can be found in the tumor. In this context the toxification (activation) kinetics of ifosfamid is discussed and an optimized, programmed infusion is considered. 5. The treatment with ifosfamid does not affect at least up to the third day the tumor hyperacidification attainable by a long-lasting glucose infusion.