Fish are subject to a variety of long and short term environmental and physical insults during their life; however they manage to adapt, ensuring physiological processes remain effective, enabling the animal to thrive in a wide range of conditions. One major environmental fluctuation that can occur rapidly or over a long period of time is temperature. Teleost fish, such as the rainbow trout (Oncorhynchus mykiss) are ectothermic, meaning their body temperature is regulated by environmental temperature which can affect activity levels, oxygen availability, biochemical reactions, biophysical processes, and importantly, circulatory demand and cardiac output.Rainbow trout heart is a relatively simple structure consisting of a single atrium and a single, double layered ventricle in an enclosed circulatory system. Cardiac output in the trout is largely intrinsically regulated in the short term by stretch, which modulates stroke volume.Long term acclimation or adaptation to cold temperature in trout has been previously shown to cause a type of cardiac remodelling, cardiac hypertrophy: an increase in muscle mass of the heart. The increase in muscle mass is thought to mitigate against the increase in blood viscosity in cold conditions.The aim of the present study was to further characterise this cardiac remodelling by using histological, immuno and genetic techniques to assess temperature dependent changes in the ventricle and atrium at the structural, proteomic and genetic levels, including defining the potential triggering events and mechanisms behind the changes. Trout were acclimated to three different temperatures. There was extensive temperature dependent, chamber specific remodelling of the muscle, connective tissue, and gap junction conduction channels. Atrial changes largely opposed ventricular responses. Cold acclimation was associated with spongy layer hypertrophy, increased collagen throughout, and atrophy of the atria. The reverse was true in warm acclimation. Genetic and proteomic analysis revealed there to be significant muscle (e.g. VMHC and MLP) and collagen (e.g. MMP13 and TIMP2) gene regulation coupled with temperature dependent changes in gap junction levels (e.g. Cx43 and Cx30.9) and distribution. Moreover, markers for stretch (e.g. ANP and BNP), stress (e.g. GR1 and DNAJ2) and neuro-hormonal input (e.g. Beta-AR2 and Beta-AR3b), coupled with significant cell signalling protein activation (e.g. p38MAPK and PKB) revealed extensive cardiac remodelling from trigger to output.Results from this study led to the conclusion that temperature acclimation causes extensive structural remodelling of the heart in order to satisfy the circulatory demand requirements of the animal in extremes of temperature. Cold fish are relatively inactive as shown by decreases in VEGF, and the heart remodels to pump blood around the body at low pressure, as shown by decreased compact layer thickness and atrophy of the atrium, and at low ejection volume, as shown by increases in stiffening collagen and spongy layer hypertrophy. A key trigger for the remodelling response is likely to be the degree of stretch the heart muscle is subject to, probably due to increased blood viscosity as shown by increases in stretch markers ANP and BNP in cold ventricle. To help ensure electrical harmony, gap junction remodelling occurs, as shown by significant changes in connexins in acclimated hearts. Due to structural observations and observed activation of signalling pathways such as GSK/PKB/NFAT, it was concluded that cardiac remodelling in rainbow trout shares similarities with physiological eccentric cardiac hypertrophy in mammals.
| Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:588134 |
| Date | January 2013 |
| Creators | Fenna, Andrew |
| Contributors | Shiels, Holly |
| Publisher | University of Manchester |
| Source Sets | Ethos UK |
| Detected Language | English |
| Type | Electronic Thesis or Dissertation |
| Source | https://www.research.manchester.ac.uk/portal/en/theses/cardiac-remodelling-in-thermally-acclimated-fish(5521e543-4587-41bb-ac23-8ce801f435ef).html |
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