Values and nursing ethics: a bibliography.
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Biomedical subjects
Publications and source records attributed to L Winkler.
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Wistar rats were fed during the whole time of gestation with a fat-free diet. The diet regime was continued for the pups and mothers after term up to day 56 post partum. Phospholipids, cholesterol, and cerebrosides were estimated in the fetal brain at the 22nd day of gestation and in the brains of the new born animals at the 14th and 56th day post partum. The molar ratios typical for mature of myeline were followed up. Fat-free diet caused a reduction of brain weight by 50 per cent in fetuses at day 22 of gestation if compared with control animals. At day 14 and 56 post partum, however, this differences has been adjusted. Within the main phase of myelinization (14th-56th day) the brains of the diet animals showed an increased accumulation of phospholipids, a lower rise in cholesterol, and a strongly depressed accumulation of cerebrosides if compared with the control group. The results support the view that the fat-free diet may lead to a persistence of early states in mature of the myeline with an enrichment in membrane structures corresponding to early myeline.
The syntheses of arachidonic acid and total fatty acids were measured in human placentas at the end of the first trimester and at term using 14C-acetate in in vitro incorporation experiments. The rates of arachidonic acid synthesis were determined to be 0.70 (first trimester) and 0.64 (term) mumol/h/100 g of placental tissue. The calculated rates of total fatty acid synthesis amount to 0.5 (first trimester) and 0.6 (term) mumol palmitate-equivalents/h/100 g. The results suggest that the human placenta seems to be not dependent on maternal arachidonic acid. Near term the placenta even could be source of arachidonic acid.
Pregnant Wistar rats were fed a fatfree diet from day 16--22 of pregnancy. On day 22, the fatty acid components of cholesterol esters, triglycerides, free fatty acids and phospholipids of maternal (brain, muscle, serum, white adipose tissue, liver) and fetal (brain, carcass, serum, liver) tissues, including the placenta, were examined gaschromatographically for the participation of linoleic and arachidonic acid. In all fetal and maternal organs the linoleic acid levels in the fatty acid patterns were strongly reduced. The alterations nearly always involved all the lipid fractions of a tissue and were mostly equal within a tissue. The strongest decreases of linoleic acid occurred in the placenta, and the weakest, in the lipids of maternal muscle and maternal adipose tissue. The linoleic acid alterations were principally similar in fetal and the corresponding maternal tissues, while being less pronounced in case of maternal muscle. The participation of arachidonic acid in the fatty acid pattern is completely retained in the lipids of fetal organs, and is even enhanced in those of the placenta.
1. Concentration and composition of the "very low density lipoproteins" (VLDL), "low density lipoproteins" (LDL) and "high density lipoproteins" (HDL) and of non-floatable lipids of fetal rat serum (day 22 of pregnancy) were determined by ultracentrifugation, thin-layer chromatographic separation of the floated lipids and quantitation of the lipid and protein moiety. 2. The concentration of VLDL is in the fetal rat by one order of magnitude lower, and that of LDL, 5fold higher than in the adult animal; the concentration of HDL in fetal serum amounts to 60% of the value of adult animals. 3. The composition of LDL and HDL of fetal serum does not differ from that in the serum of adult animals; in contrast, the fetal VLDL have a higher proportion of protein and cholesterol and a lower proportion of triglycerides than the VLDL of adult serum. The electrophoretic mobility of the fetal VLDL is lower than that of adult VLDL.
1. The semi-quantitative development of lipoproteins in the serum (beta-, pre-beta- and alpha-lipoproteins) from fetal (day 18 of intra-uterine development) to adult age was determined by agarose gel electrophoresis and determination of total lipids. 2. A high proportion of beta- and a very low proportion of pre-beta-lipoprotein is typical of the fetal stage. In adult age, however, the beta-lipoproteins are the smallest fraction, and the pre-beta-lipoproteins, the second-strongest fraction. 3. The transition from fetal to adult lipoprotein pattern is more or less abrupt, with the change of the proportion for each of the three lipoprotein fractions occurring at different intervals from birth. Adaptation of the fetal lipoprotein status to that of the adult animal in regard to quantity and mutual relationship of the fractions was observable, at the earliest, 7 weeks after birth.
The concentration and composition of the lipoprotein density classes d less than 1.006 (VLDL), d = 1.006 - 1.064 (LDL), and d = 1.064 - 1.21 (HDL) of human umbilical cord serum were investigated by means of preparative ultracentrifugation. The concentrations of all the density classes, in particular that of the VLDL, are lower than in adults; the values correspond to 8.1 (VLDL), 59.2 (LDL), and 77.4 (HDL) mg/100 ml. About 15% of the total cholesterol and roughly 40% of the total lipid phosphorus did not float at the highest density of 1.21. The composition of the LDL and the HDL was principally in agreement with the pattern obtained in adults. The VLDL of the cord serum, however, showed a lower amount of triglycerides (45%) and a higher content of proteins (22%) than the VLDL from serum of adults. In cord serum only 25% of the total triglycerides are associated with the VLDL fraction, while more than 50% of the triglycerides circulate as a constituent of the LDL.
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In rats receiving a fat-free food throughout the period of pregnancy, the individual fatty acids of total lipids from placenta, total fetus, maternal and fetal serum were determined quantitatively on day 21/22 of pregnancy. Also, the incorporation of 14C-acetate in vitro into placental fatty acids, divided by the number of double bonds, was measured and the rate of synthesis calculated therefrom. The fat-free diet caused a drastic fall of linoleic acid concentration in maternal serum and all fetal compartments. On the contrary, the amount of arachidonic acid remained almost unchanged in fetal serum and total fetus, and even slightly increased in placenta. In the maternal serum, too, the arachidonic acid concentration remained constant under fat-free diet. The observed concentration changes of single fatty acids in the maternal serum are reflected in all fetal compartments and led to a rise in total fatty acids in all sera and tissues studied. The height of rise decreased in the order: maternal serum less than placenta less than fetal serum less than total fetus. The rate of synthesis for arachidonic acid in placenta was on day 21/22 of pregnancy 0.3 (controls) and 0.5 (fat-free diet) micrometer/100 g placenta and hour, being able to cover the placenta's own need to less than one-third. The results suggest that the protection of the feto-placental unit against arachidonic acid deficiency under fat-free diet of the mother is provided mainly by a constant supply of maternal unit with arachidonic acid under normal conditions has to be ensured essentially by the mother.
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