Volume 1 Supplement 1

Abstracts of the 50th Workshop for Pediatric Research

Open Access

Propofol administration to the fetal-maternal unit preserved cardiac function in late-preterm lambs subjected to severe prenatal asphyxia and cardiac arrest

  • Matthias Seehase1, 2,
  • Patrick Houthuizen3,
  • Reint K Jellema2,
  • Jennifer JP Collins2,
  • Otto Bekers4 and
  • Boris W Kramer2
Molecular and Cellular Pediatrics20141(Suppl 1):A1

DOI: 10.1186/2194-7791-1-S1-A1

Published: 11 September 2014

Aims

Cardiac dysfunction is reported after severe perinatal asphyxia. We hypothesized that maternal propofol anaesthesia during emergency caesarean section diminished cardiac injury in preterm fetuses exposed to global severe asphyxia in utero in comparison to isoflurane anesthesia. We tested if propofol decreased the activity of pro-apoptotic caspase-3 by activating the anti-apoptotic AKT kinase family and the signal transducer and activator of transcription-3 (STAT-3).

Methods

44 late-preterm lambs underwent standardized umbilical cord occlusion (UCO) or sham-treatment in utero. UCO resulted in global asphyxia and cardiac arrest. Mothers were randomized to either propofol or isoflurane anaesthesia. After emergency caesarean section, the fetuses were resuscitated and anaesthetized for 8h by the anaesthesia of their mothers.

Results

Propofol treatment resulted 8h after UCO in reduced troponin T levels, in a higher median left ventricular ejection fraction of 84% in comparison to isoflurane (74%), and in reduced activation of caspase-3. Phosphorylated STAT-3 and AKT kinase family were increased to 655% and 500% with propofol after asphyxia.

Conclusions

Propofol administration preserved cardiac function of late-preterm lambs after asphyxia better than isoflurane. The underlying mechanism may be an activation of the anti-apoptotic STAT-3 and AKT pathway.

Authors’ Affiliations

(1)
Department for Pediatric Cardiology and Intensive Care Medicine, Georg-August-University Göttingen
(2)
Dept. of Pediatrics, Maastricht University Medical Center
(3)
Department of Physiology, Cardiovascular Research Institute Maastricht (CARIM), Maastricht University Medical Center
(4)
Department of Clinical Chemistry, Maastricht University Medical Center

Copyright

© Seehase et al; licensee Springer 2014

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.