Control of the Heart Rate in the Pre-innervated Rat Embryonic Heart
Independent thesis Advanced level (professional degree), 20 credits / 30 HE creditsStudent thesis
Oxygenation in the early mammalian embryos appears to be tightly controlled since the level of oxygenation determines blood vessel development. In so far as cardiac activity controls tissue oxygenation, embryonic heart activity also needs to be tightly controlled. Unlike the adult heart, the embryonic heart does not have an extrinsic nerve supply during most of the organogenic period so the ability to control the cardiac output must involve other mechanisms
The aims of this study were; (i) to determine at what stage of development the rat embryonic heart rate (HR) is dependent on the If current which characterises the pacemaker cells of the adult heart (ii) to test the hypothesis that the embryo contains cells that can produce and release catecholamines during hypoxia and that these catecholamines stimulate the heart to beat faster (iii) to test the hypothesis that the reduction in HR observed in rat embryos during hypoxia is due to activation of KATP channels.
These aims were studied using an in vitro system where rat embryos were maintained in short term culture under normoxic or hypoxic conditions. Their HR was monitored and then it was determined if the HR was changed by the addition of various agonists or antagonists for the various currents and ion channels mentioned above.
The use of the If channel inhibitor ivabradine on rat embryos from gestation day (GD) 10-14 showed that the rat embryonic HR is highly dependent on the If current and is dependent from almost the start of cardiac activity (GD10). The use of catecholamine agonists or antagonists on GD13 rat embryos in normoxia or hypoxia failed to demonstrate any relevant change in HR and therefore does not support the hypothesis that the early embryo can produce catecholamines to increase HR. The use of KATP agonists and antagonists on GD13 rat embryos in normoxia or hypoxia failed to demonstrate any role for these channels in the response to hypoxia.
Place, publisher, year, edition, pages
2015. , 47 p.
embryo, heart rate, hypoxia
Pharmacology and Toxicology
IdentifiersURN: urn:nbn:se:uu:diva-242075OAI: oai:DiVA.org:uu-242075DiVA: diva2:782226
Subject / course
Master of Science Programme in Pharmacy
Webster, Bill, Professor
Hellman, Björn, Professor