Letter: Beta-blockers and fibrinous peritonitis.
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Biomedical subjects
Publications and source records attributed to B T Jackson.
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Fetal bile salt metabolism was assessed by the intravenous infusion of e114C]cholate into 6 monkey fetuses. The placental transfer, fetal plasma clearance, and fetal hepatic excretion of the administered radiolabeled bile salt were measured. Placental transfer averaged 30% of the injected dose, while biliary excretion averaged 36%. Of the amount excreted by the fetal liver, 78% was in the form of [14C]taurocholate. The findings suggest that bile salt metabolic and excretory mechanisms are undergoing developmental maturation at birth.
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1. Advanced techniques for intra-uterine surgery were used to study haem degradation in foetal sheep prepared in utero with indwelling jugular, carotid and biliary cannulas. [(14)C]haemin was administered I.V. to the foetus, and plasma disappearance, biliary excretion, placental transfer and tissue distribution of radioactivity were measured over a 5-8 hr period.2. 8-30% of the (14)C-label was recovered in foetal bile, about 40% of this as bilirubin and the rest as unidentified [(14)C]haemin derivatives. 4-21% was transferred across the placenta, appearing in maternal bile almost exclusively as [(14)C]bilirubin. Excretion of (14)C-label totalled 18-33%.3. Six adult sheep infused with [(14)C]haemin excreted 19-49% of the dose in the bile over 8 hr, one third as bilirubin.4. The amount of endogenous bilirubin excreted per unit time/unit wt. of foetal liver increased with increasing foetal wt.5. It is concluded that near-term foetal sheep have a maturing mechanism for haem catabolism. Haem is partially excreted in foetal bile as bilirubin. Another fraction is transferred across the placenta, probably after prior conversion to bilirubin. The remainder is converted to un-identifiable end-products. Total excretion is approximately as effective as that in adults.
Even though certain aspects of the fetal pituitary-adrenal system have been extensively studied, much remains to be learned of its basic development and function. In the present work, the effect of maternal hypophysectomy upon quantitative pituitary-adrenal relations in mother and fetus was investigated in pregnant beagle dogs. At 57 days gestation in each of seven normal animals and seven animals 3 wk posthypophysectomy, a cannula for collection of adrenal effluent was placed in a single fetus in utero under halothane anesthesia. A timed fetal adrenal sample was obtained; ACTH (10 mU) was injected into the fetus; 3 min thereafter a second fetal adrenal sample was collected and fetal and maternal peripheral arterial samples were drawn. All fetuses and their adrenal glands were weighed. Concentrations of cortisol and corticosterone were determined by a modification of the double-isotope dilution derivative method of Kliman and Peterson. Mean peripheral cortisol concentrations in mother and fetus were 92 and 94 ng/ml, respectively (ratio 1.0), in normal pregnancies and 11 and 54 ng/ml, respectively (ratio 0.2), in maternal hypophysectomy pregnancies. Weights of fetal adrenal gland pairs of 32 and 44 mg, respectively, in normal and hypophysectomy pregnancies indicate increased fetal ACTH secretion in response to lowered circulating cortisol in the fetus secondary to maternal hypophysectomy. These data demonstrate the presence of an active pituitary-adrenal feedback mechanism in the dog fetus which is partly influenced by maternal pituitary-adrenal function. The shift in the maternal-fetal ratio of peripheral cortisol concentrations from 1.0 to 0.2 occasioned by maternal hypophysectomy neither supports nor rules out the presence of specific placental mechanisms affecting relative concentrations of cortisol in mother and fetus. It does suggest, however, that the relative steroid input into maternal and fetal compartments is one of the factors which influences such concentration ratios. Concentrations of cortisol were significantly higher in fetal adrenal effluent (pre-ACTH) than in fetal peripheral plasma in normal pregnancies, which demonstrates secretion of cortisol by the fetus and shows that corticosteroid of maternal origin does not lead to complete suppression of fetal pituitary-adrenal function. Cortisol secretion rates in response to exogenous ACTH were essentially the same in fetuses in normal and hypophysectomy pregnancies (132 and 128 ng/min, respectively). Thus, fetal adrenal responsiveness to ACTH, i.e., maximum secretory capacity, is not enhanced by increased ACTH stimulation sufficient to induce adrenal hypertrophy in the same fetuses.
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