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Fructose tolerance tests were applied to 54 piglets, aged between zero and 20 hours, two and three, five and seven, as well as 20 and 30 days. Fructose injections per kilogram of body weight were 0.5 g and 1.0 g. Galactose tolerance tests were applied to 33 piglets, aged between zero and 20 hours as well as between five and seven or 20 and 35 days. The galactose dose per kilogram of body weight was 0.5 g. Very slow or no fructose elimination at all was recordable from the circulation of animals, aged between zero and 20 hours, yet, with elimination rates being accelerated along with growing age. Piglets, aged between 20 and 30 days, eliminated fructose from the blood just as fast as glucose (th = 0.49 +/- 0.11 hr). Fructose depressed the glucose levels in the blood in animals, aged between five and seven days, but it failed to do so in animals, aged between 20 and 30 days, Galactose was found to be eliminated speedily from the circulation, that is immediately after birth, a maximum being reached at an age between five and seven days (th = 0.11 +/- 0.02 hr). Fructose space in piglets, aged between five and seven or between 20 and 30 days, was found to be significantly below that recorded from the two younger age groups. Galactose space in piglets, aged between five and seven days, was significantly below that of the other two groups.

Different groups of rats suffering from galactosamine hepatitis or ANIT-cholestasis received 200 mg galactose either by 5 minutes intravenous infusion or via a gastric tube. Blood galactose concentrations were measured for a time period of 1.5 hrs. after intravenous administration and the galactose elimination capacity (GEC) was calculated. After oral administration the galactose blood concentrations were determined for a period of 3.5 hrs. and the oral galactose clearance was estimated. After termination of both types of galactose loading the activity of the galactokinase (EC 2.7.1.6.) was determined in total liver homogenate and compared either to the GEC or to the oral galactose clearance in vivo. Galactokinase activity in the liver increased in the group of animals with experimental cholestasis and was significantly reduced in the galactosamine treated group. In vivo these changes could be estimated much better by the GEC than by determination of the oral galactose clearance.

Based on the current view about disturbances of the feto-materno-placental unit we examined 37 women with suspected intrauterine fetal growth retardation and 12 women with threatened premature labor and looked for possibilities of antenatal therapeutic influence of nutritive, respiratory, endocrine and hemodynamic insufficiency. In a randomized study we can prove a normal increase of the distance between symphysis pubis and fundus as well, as the biparietal diameter not only following bedrest but also following bedrest with additional intravenous infusion of glucose respectively oral application of galactose. The high rate of hypotrophic babies is no argument against a positive influence on nutritive insufficiency, but the acquired retardation can not be compensated totally. Neither a positive influence on the endocrine insufficiency nor the moderate respiratory one could be found. As well by maternal transcutaneous nerval stimulation as by maternal oxygen inhalation an oral long-term tocolysis we can demonstrate a considerable improvement of the uteroplacental perfusion measured with isotopes. These positive aspects are basis for further investigations. An important supposition to a successful therapy remains an early diagnosis.

The determination of the galactose elimination capacity with the method according to Tygstrup (1966) is the only test which detects the "functional hepatocyte mass" and thus constitutes a quantitative test for the metabolic function of the liver. In this determination of the maximum hepatic elimination capacity, differences with bilirubin, hemolysis and hyperlipidemia do not occur; reliable results are also obtained in disorders of hepatic secretion. Side-effects from the test substance galactose are not to be expected. It is also possible to determine galactose without difficulty in capillary blood. The i.v. galactose test permits an estimation of the degree of severity of liver diseases and can also be recommended for routine use in the investigation of specific hepatological questions.

Three lambs, aged between four and five weeks, and four sheep, aged one year, received infusions of galactose solutions (0.5 g galactose/kg body weight). The average half-life values were 28.7 minutes in the lambs and 59 minutes in the sheep. Average galactose concentrations, five minutes from mid-infusion, were 61 +/- 1.2 mg/100 ml of blood plasma in the lambs and 71 +/- 3.3 mg/100 ml in the sheep. The infusions caused statistically significant rises of glucose in the blood plasma of both lambs and sheep and an additional rise of fructose in the blood plasma of the sheep. In sheep galactose infusion resulted in rise of insulin in the blood plasma, within ten minutes from mid-infusion, the latter rise being statistically significant, from 53 +/- 26 microE/ml to 96 +/- 23.3 microE/ml. The lambs exhibited, as a result of the infusions, statistically significant rises of blood-borne lactate from 6.7 +/- 2.3 mg/100 ml to 16.7 +/- 1.2 mg/100 ml on average, within five minutes from mid-infusion.

In a randomized prospective study, performed on 45 pregnancies with clinical and sonographic suspicion for intrauterine fetal growth retardation, examinations were done to evaluate the therapeutic effect of bed rest and of additional daily administered glucose infusions or oral galactose applications respectively on the fetal growth, the hemodynamic, respiratory and endocrine insufficiency of the materno-feto-placental unit as well as selected biochemical parameters of the umbilical blood. There is no positive therapeutic effect, either on the impaired endocrine partial function nor on the reduced respiratory function of the feto-placental unit. It is obvious, that despite the improvement of the nutritional supply of the fetus and the revival of the regular fetal growth, the previous lack of fetal growth can not be altered. This can be demonstrated in all three therapeutic groups due to the fact of a resulting high hypotrophy-rate of the newborns. The results prove that the additional supply of the fetus with glucose or galactose does not remarkably improve the therapeutic effectivity as opposed by strict bed rest alone.