TY - JOUR
T1 - Fetal Stress Response to Fetal Cardiac Surgery
AU - Lam, Christopher T.
AU - Sharma, Samar
AU - Baker, R. Scott
AU - Hilshorst, Jerri
AU - Lombardi, John
AU - Clark, Kenneth E.
AU - Eghtesady, Pirooz
N1 - Funding Information:
The authors gratefully acknowledge the technical assistance of Mr. Robert Ferguson and Anoop Brar, PhD, for insightful discussions and input, Mr. Robert Giulitto and Hoxworth Blood Center for donation of blood collection supplies, and Jodie Duffy, PhD, for use of the microplate reader. Our research is supported by grants from the American Heart Association National Scientist Development Grant (0535292N), Children's Heart Foundation of Chicago, Children's Heart Association of Cincinnati, and the Cincinnati Children's Hospital Research Foundation Translational Research Initiative.
PY - 2008/5
Y1 - 2008/5
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=42949168186&partnerID=8YFLogxK
U2 - 10.1016/j.athoracsur.2008.01.096
DO - 10.1016/j.athoracsur.2008.01.096
M3 - Article
C2 - 18442572
AN - SCOPUS:42949168186
SN - 0003-4975
VL - 85
SP - 1719
EP - 1727
JO - Annals of Thoracic Surgery
JF - Annals of Thoracic Surgery
IS - 5
ER -