Biomedical subjects
Publications and source records attributed to P G Reitnauer.
In Wistar rats the sure leukopoietic effect of 165 mg/kg-1 of 2-cyanethylurea was found to be increased distinctly and in some cases significantly by doubling the O2 shares of inhaling air to 42%. Small lymphocytes are the main carrier of this effect. The potential immunological relevance of the findings is referred to.
The optimal transmission of very diluted blood samples from 11 vertebrate species and man were measured. The red cells of 10 species reduced their volume when glucose or equi-osmotic amounts of sodium chloride were added. Only the erythrocytes of man and monkey (Japanese macaques) did not reduce their volume after addition of glucose or renormalized or overcompensated minor transitory changes. This increase of the volume of human red cells is, however, too low for noticeable viscosity changes of whole blood to be caused, if any. The different response of red cells to glucose makes a simple differentiation between animal and human blood samples possible, provided that primates other than man are excluded.
Local tumor hyperthermia (42--43 degrees C) during moderate whole body hyperthermia (40 degrees C) and hyperglycemia (5 . 10(-3) g ml-1) led to an amplification of tumor hyperacidification of deltapH = 0,47 +/- 0,19 In 12 from 20 animals. As cause of this phenomenon the stimulation of glycolysis by temperature increase (van't Hoff's law) and the stop of microcirculation by hyperthermia plus decrease of erythrocyte flexibility was discussed 5 tumors regressed totally.
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Measurement on 3,4-benzopyrene- and methylcholanthrene-induced tumours of the rat (and mouse) showed that the multiple established manipulated hyperacidification of transplantation tumours to values about pH 6 is possible also on autochthonous tumours.
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.
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A discussion of physiological fundamentals with respect to the inhibition of blood microcirculation in (tumor) tissue at reduced pH values around 6.0 is followed by a report on principles, design and results obtained with a light probe array which permits to determine in vivo reference values of the relative intensity of microcirulation in both normal and tumor tissues under various conditions. An analysis of the discussed records has shown that--as compared to a value of 80-66% without glucose infusion--the relative mean intensity of microcirculation in tumor tissue drops to approximately 8-4% about 300 min after the onset of glucose infusion under CMT administration at 37 degrees C. By adding the CMT step of hyperthermy, the relative mean intensity of microcirculation--compared to normal tissue at 37 degrees C--will further drop below 1%. With such a decline of microcirculation--and an adequate duration of, say, 8 hours--local hyperthermy at 41-42 degrees C is likely to cause a very pronounced damaging action on tumor tissue because the then noticeably reduced substrate offer proves to be insufficient to ensure the structure-maintaining metabolic rate of cancer cells.
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