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An assessment of ischemia-reperfusion injury in rats exposed to chronic psychological stress

Thesis (MSc)--Stellenbosch University, 2019.

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Main Author: Oliver, Lukas Van Zyl
Other Authors: Essop, M. Faadiel
Format: Thesis
Language:en_ZA
Published: Stellenbosch : Stellenbosch University 2019
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access_status_str Open Access
author Oliver, Lukas Van Zyl
author2 Essop, M. Faadiel
author_browse Essop, M. Faadiel
Oliver, Lukas Van Zyl
author_facet Essop, M. Faadiel
Oliver, Lukas Van Zyl
author_sort Oliver, Lukas Van Zyl
collection Thesis
dc_rights_str_mv Stellenbosch University
description Thesis (MSc)--Stellenbosch University, 2019.
format Thesis
id oai:scholar.sun.ac.za:10019.1/106979
institution Stellenbosch University (South Africa)
language en_ZA
last_indexed 2026-06-10T12:43:46.817Z
license_str Other — see source repository
provenance_str_mv Harvested via OAI-PMH from SUNScholar — Stellenbosch University Repository
publishDate 2019
publishDateRange 2019
publishDateSort 2019
publisher Stellenbosch : Stellenbosch University
publisherStr Stellenbosch : Stellenbosch University
record_format dspace
source_str SUNScholar — Stellenbosch University Repository
spelling oai:scholar.sun.ac.za:10019.1/106979 An assessment of ischemia-reperfusion injury in rats exposed to chronic psychological stress Oliver, Lukas Van Zyl Essop, M. Faadiel Stellenbosch University. Faculty of Science. Dept. of Physiological Sciences. Stress (Psychology) Cardiovascular system -- Diseases Rats -- Effect of stress on Ischaemia-Reperfusion injury Hypothalamic-pituitary-adrenal axis -- Effect of stress on Wound healing -- Animal models UCTD Thesis (MSc)--Stellenbosch University, 2019. ENGLISH ABSTRACT: Cardiovascular disease remains the leading cause of death worldwide. Apart from known risk factors such as poor dietary intake, physical inactivity and smoking, chronic psychological stress is emerging as an important modifiable risk factor in the development of cardiovascular disease. The body relies on two physiological mechanisms to counter acute stressors and to achieve and/or maintain homeostasis, i.e. the hypothalamic-pituitary-adrenal axis and the autonomic nervous system. However, chronic activation of these systems can lead to the disruption of cellular and systemic processes that could potentially result in the development of neurological or psychosomatic diseases. Both chronic stress and ischemia-reperfusion injury are associated with a robust inflammatory response and the induction of oxidative stress. Does chronic psychological stress render the heart more susceptible to ischemia and reperfusion damage, and what are the role(s) of oxidative stress and inflammation in stress-related cardiac dysfunction? These questions will form the basis of this review. Following a comprehensive review, we established that chronic stress does render the heart more susceptible to damage following ischemia-reperfusion. After reviewing the mechanisms involved in both ischemia-reperfusion and chronic stress, we hypothesized that chronic stress induced inflammation and oxidative stress are major contributors in aggravated ischemia-reperfusion injury. AFRIKAANSE OPSOMMING: Kardiovaskulêre siektes is jaarliks die grootste oorsaak van dood wêreldwyd. Behalwe die bekende risikofaktore soos swak dieetinname, fisiese onaktiwiteit en rook, verskyn kroniese psigologiese stres as 'n belangrike veranderlike risikofaktor in die ontwikkeling van miokardiale infarksie. Die liggaam maak staat op twee fisiologiese meganismes om akute stressors teen te werk en homeostase te bewerkstellig of te handhaaf, naamlik die hipotalamus-pituïtêre-byniere-as en die outonome senuweestelsel. Alhoewel dit 'n gekoördineerde fisiologiese reaksie is wat homeostase handhaaf, kan kroniese aktivering van hierdie stelsel lei tot die ontwrigting van sellulêre en sistemiese prosesse wat moontlik kan lei tot die ontwikkeling van neurologiese of psigosomatiese siektes. Beide kroniese sielkundige stres en iskemie-reperfusiebesering word geassosieer met 'n sterk inflammatoriese reaksie en die induksie van oksidatiewe stres. Maak kroniese psigologiese stres die hart meer vatbaar vir skade na iskemie en reperfusie, en wat is die rol van oksidatiewe stres en inflammasie in stresverwante disfunksie van die hart? Hierdie vraag vorm die basis van hierdie oorsig. Na 'n omvattende oorsig het ons vasgestel dat kroniese stres die hart meer vatbaar maak vir skade na die induksie van iskemieherperfusie. Na die hersiening van die meganismes wat betrokke is by iskemie-reperfusie en kroniese stres, het ons die hipotese vasgestel dat kroniese stres-geïnduseerde inflammasie en oksidatiewe stres belangrike bydraers is tot die verergering iskemie-reperfusie skade. Masters 2019-11-26T12:44:51Z 2019-12-11T06:41:26Z 2021-02-01T03:00:11Z 2019-12 Thesis http://hdl.handle.net/10019.1/106979 en_ZA Stellenbosch University xii, 90 pages : maps application/pdf Stellenbosch : Stellenbosch University
spellingShingle Stress (Psychology)
Cardiovascular system -- Diseases
Rats -- Effect of stress on
Ischaemia-Reperfusion injury
Hypothalamic-pituitary-adrenal axis -- Effect of stress on
Wound healing -- Animal models
UCTD
Oliver, Lukas Van Zyl
An assessment of ischemia-reperfusion injury in rats exposed to chronic psychological stress
title An assessment of ischemia-reperfusion injury in rats exposed to chronic psychological stress
title_full An assessment of ischemia-reperfusion injury in rats exposed to chronic psychological stress
title_fullStr An assessment of ischemia-reperfusion injury in rats exposed to chronic psychological stress
title_full_unstemmed An assessment of ischemia-reperfusion injury in rats exposed to chronic psychological stress
title_short An assessment of ischemia-reperfusion injury in rats exposed to chronic psychological stress
title_sort assessment of ischemia reperfusion injury in rats exposed to chronic psychological stress
topic Stress (Psychology)
Cardiovascular system -- Diseases
Rats -- Effect of stress on
Ischaemia-Reperfusion injury
Hypothalamic-pituitary-adrenal axis -- Effect of stress on
Wound healing -- Animal models
UCTD
url http://hdl.handle.net/10019.1/106979
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