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The effect of hypoxia on the embryonic rat heart at GD 11 and GD 13 in vitro
Uppsala University, Disciplinary Domain of Medicine and Pharmacy, Faculty of Pharmacy, Department of Pharmaceutical Biosciences. Sydney University.
2013 (English)Independent thesis Advanced level (degree of Master (Two Years)), 20 credits / 30 HE creditsStudent thesis
Abstract [en]

During early pregnancy the embryo is maintained at marginal oxygen levels to facilitate blood vessel development. Small fluctuations can mean the embryo is exposed to periods of insufficient oxygen, a state called hypoxia. To maintain ideal oxygenation the activity of the embryonic heart is important and during the organogenic period it has been proposed that the embryo produces adenosine which can slow the heart and norepinephrine (NE) which can increase the embryonic heart rate (EHR). The aim of this study was (i) to determine the response of the gestational day (GD) 11 and 13 EHR, to hypoxia during the organogenic period, and (ii) to determine the effect of adenosine 1 receptor, β1-adrenergic receptor agonists and antagonists in modulating this response.


   The results showed that GD 13 rat embryos can maintain a relatively high heart rate (HR) (>200 beats per minutes) in vitro when the culture medium is in equilibrium with 95 % oxygen. When the embryos were exposed to anoxia (e.g. 0 % oxygen), a major reduction in HR was seen. On the other hand, an almost complete recovery of EHR could be seen after the embryos that were kept in 0 % oxygen were regassed with 95 % oxygen.


   Embryos on GD 11 had the same HR whether they were kept in 20%, 40 % or 95% oxygen. These finding are consistent with the GD 11 embryo being dependent on glycolysis for adenosine triphosphate (ATP) production, while the GD 13 embryo is much more dependent on oxidative phosphorylation.


  The addition of a wide range of concentrations of NE to GD 13 embryos either in normoxia (95% oxygen) or in hypoxia (20 or 0% oxygen) failed to cause any statistically significant increase in EHR. This study did not confirm a role for NE in maintaining the EHR. The addition of an adenosine agonist N-Cyclopentyladenosine (240 nM) to GD 13 embryos in normoxia (95% oxygen) caused a transient decrease (18%) in EHR, supporting the suggestion that adenosine produced during hypoxia can reduce the EHR.

  It is proposed that the reduction in EHR observed under hypoxic conditions is a consequence of reduced ATP availability. The contribution of adenosine in reducing the EHR appears to be minor and there was no evidence for a role for NE.

Place, publisher, year, edition, pages
2013. , 46 p.
National Category
Pharmaceutical Sciences
URN: urn:nbn:se:uu:diva-216485OAI: oai:DiVA.org:uu-216485DiVA: diva2:690014
Subject / course
Educational program
Master of Science Programme in Pharmacy
Available from: 2014-05-28 Created: 2014-01-22 Last updated: 2014-05-28Bibliographically approved

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