No abstract

ExtractIn rats, supplied with an adequate dietary intake of magnesium, the mean fetal magnesium concentration in plasma was 2.4 mEq/liter compared with a maternal concentration of 1.6 mEq/liter. Equilibrium dialysis experiments resulted in a disappearance of the fetal to maternal gradient, with maternal levels becoming slightly higher than fetal levels. Determination of ultrafiltrable magnesium concentrations also demonstrated a slightly lower binding capacity for magnesium in fetal plasma so that the fetal to maternal gradient reflected the unbound magnesium.When a diet containing magnesium in a concentration of 0.88 mEq/kg (compared with a control diet containing 120 mEq/kg) was introduced on day 2 of gestation, only one of eight pregnant rats bore a litter to term. If the diet was introduced on day 10 of gestation, pregnancy continued until term but there was an increased resorption rate and the surviving fetuses were small, weak, and anemic. Analyses of maternal muscle for magnesium, calcium, sodium, and potassium revealed normal concentrations, even though magnesium concentrations in plasma rapidly fell to 20% of the normal level. There appeared to be a reduction in bone magnesium. The significant changes in the fetus were a reduction in magnesium levels in plasma with a disappearance of the fetal to maternal gradient and an elevation in sodium levels. Analysis of the total fetus demonstrated a reduction in magnesium and potassium and an increase in calcium concentrations. The last was also evident in the placenta. Speculation"Fetal parasitism" as a general concept appears to be. an over-simplification which can be denned with accuracy only by the study of deprivations of specific nutrients, and eventually by the interaction of such nutrients.

Maternal rats fed a diet deficient in potassium (K) during pregnancy were depleted of K so that the plasma level of K fell to one-half the normal value and the concentration in maternal muscle fell by about 30%. The K concentration in fetal plasma under these circumstances did not change significantly, but that in fetal tissues (placenta and fetus) decreased by roughly 10% ( fig. 1, table III). Maternal hyperkalemia, induced by a sodium-deficient diet or produced by infusions of K (table IV) induced a fetal hyperkalemia ( fig. 1). Maternal hyponatremia caused proportional hyponatremia in the fetus (slope = 0.60, correlation coefficient = 0.91) (fig. 2); the sodium content of the fetus was also reduced in maternal hyponatremia ( fig. 3). SpeculationDeserving of particular emphasis is the contrast between the effect of maternal hyperkalemia and hypokalemia on the level of potassium in the fetal blood. This difference in response raises questions concerning the mechanism of placental transport of potassium. It would be of interest to determine if the placenta protects the fetus against other maternal ion deficiencies. Introductionthe mother is subjected to the severe stress that results from specific nutritional deficiencies. The present Mammalian pregnancy offers the fetus the advantage studies concentrate on the effects of potassium (K) of a controlled environment during a critical period of and sodium (Na) deficiences. Acute elevations of K growth and development. The control is provided levels in the plasma of the mother were also induced primarily by the homeostatic mechanisms of the because of questions raised by some of the nutritional mother which maintain the composition of her blood, studies. under normal conditions, within relatively narrowThe rat was chosen as the experimental animal belimits. It is suspected that the placenta, through its cause extensive nutritional information about this array of active transport mechanisms, may serve as a animal was already available, because of the ease of second line of defense.obtaining modified diets, and because the rapid rate These investigations have been designed to study of growth of the total fetal mass presents particularly the mechanisms by which the fetus is protected when severe demands on the dam.

SUMMARY The fatty acid distribution in the lipids from certain raw and cooked variety meats was determined with gas‐liquid chromatography. The method of cooking utilized moist heat (braising) in all cases. Fatty acid distribution was not significantly changed by cooking. Beef kidney, beef and pork liver, and beef heart fatty acids contained 25‐36% of polyunsaturated fatty acid:. Distributions of the major fatty acids (as percent of total fatty acid) were generally as follows. Beef kidney: palmitic acid, 17; stearic acid, 19; oleic acid, 21; linoleic acid, 19; and arachidonic acid, 14. Beef liver: palmitic acid, 13; stearic acid, 34; oleic acid, 14; linoleic acid, 11; arachidonic acid, 7; and docosahexaenoic acid (C22‐hexaene), 6. Pork liver: palmitic acid, 21; stearic acid, 26; oleic acid, 22; linoleic acid, 13; and arachidonic acid, 12. Beef heart: palmitic acid, 13; stearic acid, 17; oleic acid, 18; linoleic acid, 25; and arachidonic acid, 11. Beef tongue: palmitic acid, 28; stearic acid, 11; oleic acid, 44; linoleic acid, 4; and arachidonic acid, 2. These results indicate that certain of the variety meats may be excellent sources of polyunsaturated fatty, acids. Pork and beef liver differed significantly in docosahexaenoic acid and arachidonic acid content.