ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Ann Thorac Surg 2008;85:1719-1727. doi:10.1016/j.athoracsur.2008.01.096
© 2008 The Society of Thoracic Surgeons
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Author home page(s):
John Lombardi
Pirooz Eghtesady
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Google Scholar
Right arrow Articles by Lam, C. T.
Right arrow Articles by Eghtesady, P.
PubMed
Right arrow Articles by Lam, C. T.
Right arrow Articles by Eghtesady, P.
Related Collections
Right arrow Cardiac - physiology
Right arrow Extracorporeal circulation
Right arrowRelated Article

Original Articles: Pediatric Cardiac

Fetal Stress Response to Fetal Cardiac Surgery

Christopher T. Lam, BSa, Samar Sharma, BSa, R. Scott Baker, BSa,b, Jerri Hilshorst, CCPa, John Lombardi, CCPa, Kenneth E. Clark, PhDb, Pirooz Eghtesady, MD, PhDa,b,*

a Division of Cardiothoracic Surgery, Cincinnati Children's Hospital Medical Center, Cincinnati, Ohio
b Department of Obstetrics and Gynecology, University of Cincinnati, Cincinnati, Ohio

Accepted for publication January 28, 2008.

* Address correspondence to Dr Eghtesady, Division of Cardiothoracic Surgery, Cincinnati Children's Medical Center, 3333 Burnet Ave, Cincinnati, OH 45229-3032 (Email: pirooz.eghtesady{at}cchmc.org).

Background: A deleterious fetal stress response, although not fully elucidated, may account for poor outcomes after experimental fetal cardiac surgery. We set out to characterize this fetal stress response and its potential role in placental dysfunction.

Methods: Fifteen ovine fetuses at gestational day 100 to 114 were placed on extracorporeal support for 30 minutes and were then followed 2 hours after cardiopulmonary bypass. Fetal plasma samples were analyzed for vasopressin, cortisol, and β-endorphin levels, and correlated to fetal hemodynamics and placental gas exchange.

Results: Unique temporal patterns of response were seen in release of the three stress hormones. Vasopressin demonstrated the most profound and early response followed by cortisol and β-endorphin, the latter continuing to rise in the post-bypass period. A sharp rise in fetal mean arterial pressure and placental vascular resistance strongly correlated with rising vasopressin levels. Post-bypass deterioration of fetal gas exchange and hemodynamics correlated with the ensuing rise in cortisol and β-endorphin. Rising fetal lactate levels correlated with elevations in all three stress hormones.

Conclusions: Fetal cardiopulmonary bypass leads to a profound, early rise in vasopressin concentrations that strongly correlates with placental dysfunction after fetal bypass. Vasopressin may play an important mechanistic role in pathogenesis of this placental dysfunction.


Related Article

Invited Commentary
Kathleen N. Fenton
Ann. Thorac. Surg. 2008 85: 1727-1728. [Extract] [Full Text] [PDF]



This article has been cited by other articles:


Home page
 Ann. Thorac. Surg.Home page
K. N. Fenton
Invited commentary.
Ann. Thorac. Surg., May 1, 2008; 85(5): 1727 - 1728.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS
Copyright © 2008 by The Society of Thoracic Surgeons.