Skip Navigation

Cardiovascular Research 2003 58(1):162-169; doi:10.1016/S0008-6363(02)00844-1
© 2003 by European Society of Cardiology
This Article
Right arrow Full Text Freely available
Right arrow FREE Full Text (PDF) Freely available
Right arrow E-letters: Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when E-letters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to My Personal Archive
Right arrow Download to citation manager
Right arrowRequest Permissions
Right arrow Disclaimer
Google Scholar
Right arrow Articles by Anim-Nyame, N.
Right arrow Articles by Steer, P. J.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Anim-Nyame, N.
Right arrow Articles by Steer, P. J.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2003, European Society of Cardiology

Microvascular permeability is related to circulating levels of tumour necrosis factor-{alpha} in pre-eclampsia

Nick Anim-Nyamea,*, John Gambleb, Suren R. Soorannaa, Mark R. Johnsona and Philip J. Steera

aDepartment of Maternal and Fetal Medicine, Faculty of Medicine, Imperial College of Science, Technology and Medicine, Chelsea and Westminster Hospital, 369 Fulham Road, London SW10 9NH, UK
bSchool of Sport and Exercise Sciences, University of Birmingham, Birmingham B15 2TT, UK

* Corresponding author. Tel.: +44-208-846-7895; fax: +44-208-846-7796. n.anim{at}ic.ac.uk

Introduction: The mechanism for the increased microvascular permeability which, underline many of the complications of pre-eclampsia, remain unexplained. It has been suggested that a factor present in the maternal circulation in pregnancies complicated by the disease may be responsible for increased microvascular permeability. In this study, we have investigated the relationship between filtration capacity (Kf), an index of microvascular permeability, and maternal levels of VEGF, leptin and TNF-{alpha}, all of which are known permeability factors whose plasma levels are increased in pre-eclampsia. Methods: We used a small cumulative pressure step venous congestion plethysmography protocol to compare Kf, an index of microvascular permeability, during the third trimester of 20 women with pre-eclampsia, 18 normal pregnant women and 18 non-pregnant female matched controls. Blood samples were obtained to measure plasma levels of VEGF, leptin, TNF-{alpha} plasma protein concentrations and full blood count. Results: Microvascular filtration capacity (Kf) was significantly increased in pre-eclampsia compared to the other groups (P<<0.0001, ANOVA). Kf was also increased in the normal pregnant group when compared to the non-pregnant controls (P = 0.02). Plasma levels of VEGF, leptin and TNF-{alpha} were significantly greater in pre-eclampsia compared to normal pregnancy and non-pregnant controls (P<0.0001, ANOVA, for all three analyses). Total plasma protein and albumin concentrations were significantly lower in the normal pregnant and pre-eclamptic groups, compared to the non-pregnant controls (P<0.0001, ANOVA). Kf was significantly related to TNF-{alpha} in pre-eclampsia (r = 0.53, P = 0.018), and with VEGF in the non-pregnant controls (r = 0.6, P = 0.02). No significant relationship was observed between Kf and VEGF, leptin and TNF-{alpha} during normal pregnancy. There was a significant inverse correlation between plasma albumin concentration and filtration capacity in the normal pregnant (r = –0.94, P<0.0001) and non-pregnant (r = –0.87, P<0.0001) groups but not in the women with pre-eclampsia (r = –0.18, P = 0.8). Conclusions: These data show that that microvascular filtration capacity is significantly increased in pre-eclampsia, and correlates with circulating levels of TNF-{alpha} but not leptin or VEGF.

KEYWORDS Growth factors; Microcirculation


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
HypertensionHome page
S. K. Walsh, F. A. English, E. J. Johns, and L. C. Kenny
Plasma-Mediated Vascular Dysfunction in the Reduced Uterine Perfusion Pressure Model of Preeclampsia: A Microvascular Characterization
Hypertension, August 1, 2009; 54(2): 345 - 351.
[Abstract] [Full Text] [PDF]


Home page
Reproductive SciencesHome page
Yang Gu, D. F. Lewis, J. S. Alexander, and Yuping Wang
Placenta-derived Chymotrypsin-like Protease (CLP) Disturbs Endothelial Junctional Structure in Preeclampsia
Reproductive Sciences, May 1, 2009; 16(5): 479 - 488.
[Abstract] [PDF]


Home page
ReproductionHome page
W Zammiti, N Mtiraoui, H Khairi, J-C Gris, W Y Almawi, and T Mahjoub
Associations between tumor necrosis factor-{alpha} and lymphotoxin-{alpha} polymorphisms and idiopathic recurrent miscarriage
Reproduction, March 1, 2008; 135(3): 397 - 403.
[Abstract] [Full Text] [PDF]


Home page
Am. J. Pathol.Home page
C. J. Lockwood, P. Matta, G. Krikun, L. A. Koopman, R. Masch, P. Toti, F. Arcuri, S.-T. J. Huang, E. F. Funai, and F. Schatz
Regulation of Monocyte Chemoattractant Protein-1 Expression by Tumor Necrosis Factor-{alpha} and Interleukin-1{beta} in First Trimester Human Decidual Cells: Implications for Preeclampsia
Am. J. Pathol., February 1, 2006; 168(2): 445 - 452.
[Abstract] [Full Text] [PDF]


Home page
J. Immunol.Home page
J. Berman, G. Girardi, and J. E. Salmon
TNF-{alpha} Is a Critical Effector and a Target for Therapy in Antiphospholipid Antibody-Induced Pregnancy Loss
J. Immunol., January 1, 2005; 174(1): 485 - 490.
[Abstract] [Full Text] [PDF]



Disclaimer: Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.