Skip Navigation

Cardiovascular Research 2003 60(1):156-164; doi:10.1016/S0008-6363(03)00338-9
© 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 Rounioja, S.
Right arrow Articles by Hallman, M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Rounioja, S.
Right arrow Articles by Hallman, M.
Social Bookmarking
Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Copyright © 2003, European Society of Cardiology

Intra-amniotic lipopolysaccharide leads to fetal cardiac dysfunction

A mouse model for fetal inflammatory response

Samuli Rouniojaa, Juha Räsänenb, Virpi Glumoffa, Marja Ojaniemia, Kaarin Mäkikalliob and Mikko Hallmana,*

aDepartment of Pediatrics and Biocenter Oulu, University of Oulu, P.O. Box 5000, FIN-90014 Oulu, Finland
bDepartment of Obstetrics and Gynecology, University of Oulu, P.O. Box 5000, FIN-90014 Oulu, Finland

*Corresponding author. Tel.: +358-8-315-5100; fax: +358-8-315-5559. Email address: mikko.hallman{at}oulu.fi

Objective: Intrauterine infection is associated with increased lipopolysaccharide (LPS) and proinflammatory cytokines in amniotic fluid. We hypothesized that intra-amniotic LPS launches a fetal inflammatory response leading to cardiac dysfunction. Methods: A mouse model was established. At 15–16 days of gestation, 52 fetuses of nine dams received LPS and 46 fetuses of nine dams vehicle intra-amniotically. Five dams underwent a sham operation. Echocardiography was performed before and 6 h after the injection to obtain inflow and outflow blood velocity waveforms. Outflow mean velocity (Vmean) and the proportions of isovolumetric relaxation (IRT%) and contraction (ICT%) times of the cardiac cycle were calculated. Pulsatility indices (PI) were calculated from the umbilical and intracranial arteries and the descending aorta. Pulsatility indices for veins (PIV) were obtained from ductus venosus. Toll-like receptor-4 (TLR4) and several other inflammatory mediators were determined using ELISA, immunohistochemistry, or ribonuclease protection assay. Results: In the LPS group, outflow Vmean was significantly lower, and ICT% and IRT% longer than in the other groups. LPS increased PIs, except in the intracranial arteries, which showed a decrease in PIs. In ductus venosus, PIVs were increased after LPS. LPS increased interleukin (IL)-6 in amniotic fluid and induced the expression of proinflammatory cytokines in placenta and fetal membranes, but not in lung. In fetal myocardium, TLR4 was constitutional. LPS induced the expression of IL-1β and tumor necrosis factor (TNF)-{alpha} mRNA in myocardium, whereas inducible nitric oxide synthase (NOS2) protein and nitrotyrosine remained undetectable. Conclusions: As a response to endotoxin in amniotic fluid, fetal myocardium acutely generates cytokines and severe fetal cardiovascular compromise develops. These two may be linked through a mechanism that does not include NO.

KEYWORDS Contractile function; Cytokines; Endotoxins; Hemodynamics; Infection/inflammation

Time for primary review 34 days.


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
 Reproductive SciencesHome page
Yafeng Dong, Weijian Hou, Jiaxue Wei, and C. P. Weiner
Chronic Hypoxemia Absent Bacterial Infection Is One Cause of the Fetal Inflammatory Response Syndrome (FIRS)
Reproductive Sciences, July 1, 2009; 16(7): 650 - 656.
[Abstract] [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.