Table of Contents Author Guidelines Submit a Manuscript
Infectious Diseases in Obstetrics and Gynecology
Volume 11, Issue 2, Pages 101-104
http://dx.doi.org/10.1080/10647440300025505

The Bidirectional Transfer and Fetal Vascular Pressure Changes Due to the Presence of 125I-Labeled Inhibin A in the ex-vivo Human Placental Model

1Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas 75390-9032, TX, USA
2Cancer Immunobiology Center, University of Texas Southwestern Medical Center, Dallas, TX, USA

Received 30 August 2002; Accepted 25 September 2002

Copyright © 2003 Hindawi Publishing Corporation. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Objective: 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 I125 -labeled synthetic glycoprotein.

Methods: Synthetic inhibinAwas 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 NaI125 process yielded I125 -labeled inhibin A with a radioactivity of106 cpm/μg. This compound was placed in the human placenta in maternal–fetal and fetal–maternal studies using antipyrine and C14 -labeled inulin as controls to determine the bidirectional transfer of the compound.

Results: 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.

Conclusions: 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.