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.
The measurements were accomplished by using an experimental setup in which an intestinal loop with adjacent mesentery of an anaesthetized rat was immersed in a buffer-containing cuvette. After i.v. injection of Evans' Blue (EB) the extravasation of the dye, which is bound to plasma albumin, was measured colorimetrically. From the curves recorded it could be derived that after i.v. injection of 2 or 4 g or infusion of 6 g/h glucose (Gk) per kg body weight the permeation of albumin-bound EB was increased by a factor of about 1.9, 3.1 and 2.0 respectively. As mechanism of these effects it is assumed that Gk (but also galactose and saccharose in control experiments) act by osmotically shrinking the endothelial cells and opening their junctions.
On rats hypothermia of 22 to 20 degrees C and rewarming to normal body temperature leads to an amplification of the hyperglycemic tumor acidification. Mechanism and significance of this effect are discussed.
One hind leg each of 20 rats was perfused by a buffer-electrolyte mixture at a rate of 1.2 ml/min. When the pH of the solution was lowered from 7.4 to 7.0 and, thereafter, to around 6.0, the mean perfusion pressure increased by 1.6 to 3.4 and 2.5 to 12.4 kPa, respectively. The higher values were obtained when the perfusate contained 2.5% dextran (m.w. 40,000). Swelling of endothelial cells and vasoconstriction are discussed as possible effector mechanisms.
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In the mesenterium of rats it was found that an overacidity of the blood flowing in the area of microcirculation and caused by irrigation with acid media may be objectively represented in the clearing of venols measurable by means of video technique. The cause of this clearing process is the swelling of erythrocytes setting in at lower pH-values. According to in-vitro findings this swelling of erythrocytes will lead to an increase of the apparent viscosity of the blood fluid or blood cell suspension respectively in conformity with the increase of hematocrit connected with it.
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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.