No abstract

No abstract

We have used instant thin-layer chromatography and radioimmunoassay to measure the concentrations of total cortisone (E) and cortisol (F) in the fetal and maternal compartments of the rabbit. The concentration of F in fetal blood increased markedly at day 25; this is just prior to the rapid increase in the surfactant phospholipids in lung tissue in this species. This increase coincided with a peak in the concentration of E and F in the maternal blood and may reflect the maternal levels. There was no ‘surge’ in the concentration of total F in fetal blood at term. The concentration of E in fetal blood varied between 5 and 15 ng/ml during this last stage of gestation, hence providing ready substrate for the 11β-reductase present in lung and other tissues. The concentration of E and F in maternal blood was significantly higher and more variable than that in blood from nonpregnant female rabbits, and there was a pronounced peak in concentration at day 30 (term: 31 days). The concentrations of both E and F in amniotic fluid were lower than those in either maternal or fetal blood until day 30 when the concentration of F increased fivefold to 19.2 ± 2.58 (mean ± SEM of 6 samples).

We have used the isolated perfused lung (IPL) preparation from the rat to determine whether uptake of choline from the vascular compartment could limit the rate of synthesis of phosphatidyl-choline (PC). The uptake of choline was rapid and did not saturate at a concentration of 10 mM. The rate of incorporation of choline into phospholipid was saturated above 0.1 mM choline. Whereas, uptake and incorporation were depressed at 4 C, uptake was neither dependent on the extracellular sodium concentration nor inhibited by equimolar concentrations of hemicholinium-3 (HC-3). We could find no evidence that uptake might limit synthesis of lung lecithin and conclude that uptake is either by free diffusion, or by a carrier-mediated process with a very high Km.