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Fetal perfusion

S. Kertschanska, G. Kosanke, and P. Kaufmann. Pressure dependence of so-called transtrophoblastic channels during fetal perfusion of human placental villi. Microsc Res Tech. 38 52-62 (1997). [Pg.387]

Fetal Perfusion. As soon as the saline perfusion is started, there are indications of the adequacy of the fetal perfusion a high fetal pressure at a low fetal flow rate indicates that many capillaries are clotted. In this case, the remaining capillaries rupture and fluid transfers from the fetal to the maternal side at a high rate. Distribution of dye in the fetal circulation was also used to check the completeness of the fetal perfusion. [Pg.188]

Pregnenolone is extensively metabolized by the different fetal tissues. After fetal perfusion, this compound is transformed into pregnenolone sulfate in all the fetal tissues, into 17a-hydroxypregnenolone, dehydroepian-drosterone, and deliydmepiandrosterone sulfate principally in the adrenal tissues, and into 20a-dihydropregnenolone and 20a-dihj dropregiienolone sulfate mainly in fetal liver (Solomon et al 1907). [Pg.171]

It is interesting to note that in contrast to experiments using fetal perfusion with pregnenolone sulfate, studies in which this ester sulfate was incubated with homogenates of fetal adrenals produced a conversion of 8.5% to 17 -hydroxyprognenolone sulfate, 1.4% to dehydroepiandrosterone sulfate and 1.1% to 16a-hydroxydehydroopiandrosterono sulfate (Perez-Palacios ei al., 1968). [Pg.175]

The 16a-hydroxylation by fetal adrenals for pregnenolone and progesterone is very active. After fetal perfusion or incubation, pregnenolone and progesterone are converted into their respective 16a-hydroxy derivatives (D. B. Villee et al., 1961 D. B. Villee and Driscoll, 1965 Solomon el al., 1967). The 16a- and 17a-hydroxylases are also very active for progesterone in fetal testis (E. Bloeli, 1964 Ikonen and Xiemi, 1966). [Pg.177]

In the fetal compartment dehydroepiandrosterone is largely converted into its 3 (J-.sulfate. After fetal perfusion with labeled dehydroepiandrosterone, 60-80% of the radioactivity of the adrenal tissues was present as dehydroC[)iandrosteroiie sulfate. These value.s dropped to 30-50% in the other fetal tissues (Boltb et at., 1966 Wengle, 1964, 1966). [Pg.193]

There is practically no sulfatase activity in the fetal compartment, and after simultaneou.s fetal perfusion of dohydroepiandrosterone- H and dehydroepiandrosterone- C-su fate, 9.")-100% of the KH-labeled material was found as ester sulfate in the different fetal tissues (Bolt et aL, 1966). [Pg.193]

Estriol was also found to circulate as 16a-ghiciiromde, 3-glucuronide, 3,16o -dig ueuronide, or as a mixed form of estriol sulfoglueuronide. After fetal perfusion with estriol, 15-20% of the radioactive material in the liver and intestinal tissues was recovered as glueuronides (Mikhail et ai., 1963b). [Pg.208]

J. Kraemer, J. Klein, A. Lubetsky, and G. Koren. Perfusion studies of glyburide transfer across the human placenta Implications for fetal safety. Am J Obstet Gynecol. 195 270-274 (2006). [Pg.388]

Perfusion of human fetal heart with anti-52-kDa Ro results in AV block (B22). [Pg.152]

In addition, the metabolic effects of insulin ultimately increase fetal oxygen consumption. The circulation of the fetus is unique specifically, because blood in the fetal descending aorta contains a portion of venous return after tissue perfusion, the increased rate of consumption of oxygen by fetal tissues decreases the arterial oxygen concentration of the fetus. The fetal tissues supplied by this circulation (which include most of the mass of the fetus) are then at risk for inadequate tissue oxygenation. [Pg.115]

Dancis J, Lehanka J, Levitz M. Placental transport of riboflavin differential rates of uptake at the maternal and fetal surfaces of the perfused human placenta. Am J Obstet Gynecol 1988 158 204-10. [Pg.1147]

Salient features of the hibernating myocardium are the increase in glucose uptake out of proportion to coronary flow (metabolism/perfusion mismatch)81 and the increase in myocardial glycogen content with ultrastructural characteristics resembling those of the fetal heart.82... [Pg.25]

A wide variety of data firom many laboratories indicates that the liver is a major source of somatomedin peptides. This has been demonstrated directly in studies of isolated perfused livers (F3, K13, MIO, P9, S9, S2I, W6), fetal (D14, R5) and adult (B25, S13) liver in organ culture, rat liver cell lines (M5, M26, S27), and primary hepatocyte cultures (K14, S22, S28). Tliese studies are supported by the observations that partial hepatectomy (U3) or liver disease (S14, T5) results in low circulating somatomedin activity. It has not always been clear, however, which members of the somatomedin family were being assayed in some of these studies, due to the broad specificity of the assays used (see Section 5). For example, whereas it has been well established that the BRL (buffalo rat liver) cell line, and fetal rat liver in organ culture (R5), produce peptides of the MSA or IGF-II family (M5, M26), it is not known whether normal adult liver produces IGF-II. Indeed, production of SM-G/IGF-I by adult liver has been demonstrated specifically in only two studies. In these, Schwander et al. (S21) found that a S-labeled product from perfused liver could be immunoprecipitated with an IGF-I antiserum, and Scott et al. (S22) used a specific SM-C/IGF-I RIA to demonstrate production of the peptide by adult hepatocytes in primary culture. In both studies, the measured hepatic production rate was calculated to be sufficient to account fully for circulating SM-C/IGF-I levels. [Pg.53]

It has been shown that the fetal adrenal can convert progesterone and pregnenolone into cortisol in substantial yield (Sections 4.2.1 and 4.2.2), and, notably, Solomon (S25), after perfusion of fetuses with proges-terone-4- C, has isolated radioactive corticosterone and cortisol from the... [Pg.165]

Effects of Varying Umbilical Flow Rate. The fetal circulation of the cotyledon was perfused at flow rates from 0.22-2.6 ml/min in sheep and from 0.05-2.3 ml/min in rabbits. About ten different flow rates were studied randomly in each of five ewes and five rabbits (47). [Pg.130]


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See also in sourсe #XX -- [ Pg.180 ]




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