The bidirectional transfer and fetal vascular pressure changes due to the presence of 125I-labeled inhibin A in the ex-vivo human placental model

The purpose of this study was to investigate the transport of inhibin A and to determine its effects on fetal vascular pressure at elevated levels in the human placenta using 125I-labeled synthetic glycoprotein. Synthetic inhibin A was prepared and was shown to be consistent with the natural form by...

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Bibliographic Details
Published in:Infectious diseases in obstetrics and gynecology 2003, Vol.11 (2), p.101-104
Main Authors: Bawdon, Roger E, Ghetie, Victor
Format: Article
Language:English
Subjects:
Chromatography, High Pressure Liquid
Female
Fetal Blood - metabolism
Gas Chromatography-Mass Spectrometry
Humans
In Vitro Techniques
Inhibins - metabolism
Iodine Radioisotopes
Maternal-Fetal Exchange
Molecular Weight
Placenta - blood supply
Placenta - metabolism
Pregnancy
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Summary:The purpose of this study was to investigate the transport of inhibin A and to determine its effects on fetal vascular pressure at elevated levels in the human placenta using 125I-labeled synthetic glycoprotein. Synthetic inhibin A was prepared and was shown to be consistent with the natural form by high-pressure liquid chromatography (HPLC) and molecular weight determination by gas-chromatography mass spectrometry. The standardized Na125I process yielded 125I-labeled inhibin A with a radioactivity of 10(6) cpm/microg. This compound was placed in the human placenta in maternal-fetal and fetal-maternal studies using antipyrine and 14C-labeled inulin as controls to determine the bidirectional transfer of the compound. Maternal-fetal and fetal-maternal clearance indices were 0.045 +/- 0.003 and 0, respectively. In eight placentas there was no evidence of vascular pressure changes due to the presence of up to 5000 pg of inhibin A. There is minimal maternal-fetal transfer and no detectable fetal-maternal transfer in normotensive and pregnancy-induced hypertensive placentas. In addition, there are no pressure changes in the fetal vascular system due to the clinically significant levels of inhibin A.
ISSN:1064-7449
1098-0997
DOI:10.1080/10647440300025505