Document Detail


Utero-placental haemodynamics in the pathogenesis of pre-eclampsia.
MedLine Citation:
PMID:  19497617     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Pre-eclampsia is associated with insufficient adaptations of spiral arteries which theoretically alter haemodynamics within the intervillous space. Such changes could damage the syncytiotrophoblast and release factors which instigate maternal endothelial dysfunction. We tested this hypothesis using an in vitro dual perfusion model of the human placenta, representing putative changes in flow arising from these spiral artery maladaptations. Whilst fetal-side flow rates remained constant (6 ml/min) perfusion rates on the maternal side were increased from 14 ml/min to 45 ml/min. As well as increasing placental derived intervillous hydrostatic pressures, and changes in flow dynamics observed by colour Doppler, these elevated flow rates resulted in morphologic damage, vacuolation and shedding of the syncytiotrophoblast, focal features previously defined in pre-eclampsia. The collected maternal perfusates recovered under high flow conditions also contained significantly elevated levels of biochemical markers of syncytial damage, including lactate dehydrogenase, alkaline phosphatase and human chorionic gonadotrophin. There were also significant elevations in chemokines GROalpha and RANTES, compared with the low flow perfusions. The soluble components of the maternal high flow rate perfusions decreased the number and proliferation of HUVECs after 24h exposure. These results could not be attributed to GROalpha or RANTES alone or in combination. This study provides evidence that alterations in intervillous flow have the potential to influence both the integrity of the syncytiotrophoblast and the liberation of potentially pathogenic soluble factors. This therefore offers a putative link between utero-placental maladaptations in pregnancy and the vascular endothelial complications of pre-eclampsia.
Authors:
E S Hutchinson; P Brownbill; N W Jones; V M Abrahams; P N Baker; C P Sibley; I P Crocker
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Publication Detail:
Type:  In Vitro; Journal Article; Research Support, Non-U.S. Gov't     Date:  2009-06-03
Journal Detail:
Title:  Placenta     Volume:  30     ISSN:  1532-3102     ISO Abbreviation:  Placenta     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2009-06-22     Completed Date:  2009-08-27     Revised Date:  2014-03-14    
Medline Journal Info:
Nlm Unique ID:  8006349     Medline TA:  Placenta     Country:  England    
Other Details:
Languages:  eng     Pagination:  634-41     Citation Subset:  IM    
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MeSH Terms
Descriptor/Qualifier:
Alkaline Phosphatase / metabolism
Apoptosis / physiology
Biological Markers / metabolism
Blood Flow Velocity / physiology*
Cell Division / physiology
Cell Survival / physiology
Cells, Cultured
Chemokine CCL5 / metabolism
Chemokine CXCL1 / metabolism
Chorionic Gonadotropin / metabolism
Endothelial Cells / cytology*,  physiology
Female
Humans
Hydrostatic Pressure
L-Lactate Dehydrogenase / metabolism
Laser-Doppler Flowmetry
Placental Circulation / physiology*
Pre-Eclampsia / etiology*,  pathology,  physiopathology*
Pregnancy
Trophoblasts / physiology
Umbilical Veins / cytology*
Grant Support
ID/Acronym/Agency:
PDA/01/05/007//Department of Health; //Medical Research Council
Chemical
Reg. No./Substance:
0/Biological Markers; 0/CCL5 protein, human; 0/CXCL1 protein, human; 0/Chemokine CCL5; 0/Chemokine CXCL1; 0/Chorionic Gonadotropin; EC 1.1.1.27/L-Lactate Dehydrogenase; EC 3.1.3.1/Alkaline Phosphatase

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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