Persistent Link:
http://hdl.handle.net/10150/282447
Title:
Metabolic aspects of neonatal rat cardiomyocyte hypertrophy
Author:
Shirazi, Farshad, 1963-
Issue Date:
1997
Publisher:
The University of Arizona.
Rights:
Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
Abstract:
The consensus view is that cardiac hypertrophy is an adaptive response to increased work caused by a variety of stimuli. While hypertrophy can be defined as an increase in cell mass without an increase in cell number, not all increases are equivalent in type and amount of protein accumulated. Our goal in this study was to identify the common steps in the process of cardiac hypertrophy. Our working hypothesis was that in all forms of cardiac hypertrophy glucose utilization increases and that the percentage of energy derived from fatty-acid oxidation decreases. The first part of this study entailed the development and characterization of a neonatal rat heart cell model. The model had to provide uniform culture conditions for rapid development of hypertrophy by agents acting at different sites in the cardiomyocytes. The second part of this study was composed of an assessment of hypertrophy caused by four pharmacologically distinct agents: norepinephrine, angiotensin-II, endothelin-I and tetradecylglycidic acid. In this part we compared the quantity of protein accumulation and quality of hypertrophy cause by each agent. This task was accomplished by examining the effect of each agent on selected mRNA messages and alteration in DNA content of cardiomyocytes. Here we also examined the effect of protein kinase-C, endothelin-I and angiotensin-II inhibitors on hypertrophy caused by each agent. In the final part of this study, metabolic alteration in hypertrophy caused by each agent was assessed for a potential common pathway to hypertrophy. As part of this analysis, we examined changes in glucose and palmitate oxidation, glucose uptake and role of pentose pathway in hypertrophy resulting from treatment of cardiomyocyte by each agent.
Type:
text; Dissertation-Reproduction (electronic)
Keywords:
Health Sciences, Toxicology.; Health Sciences, Pharmacology.; Biology, Animal Physiology.; Health Sciences, Pathology.
Degree Name:
Ph.D.
Degree Level:
doctoral
Degree Program:
Graduate College; Pharmacology and Toxicology
Degree Grantor:
University of Arizona
Advisor:
Davis, Thomas P.

Full metadata record

DC FieldValue Language
dc.language.isoen_USen_US
dc.titleMetabolic aspects of neonatal rat cardiomyocyte hypertrophyen_US
dc.creatorShirazi, Farshad, 1963-en_US
dc.contributor.authorShirazi, Farshad, 1963-en_US
dc.date.issued1997en_US
dc.publisherThe University of Arizona.en_US
dc.rightsCopyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.en_US
dc.description.abstractThe consensus view is that cardiac hypertrophy is an adaptive response to increased work caused by a variety of stimuli. While hypertrophy can be defined as an increase in cell mass without an increase in cell number, not all increases are equivalent in type and amount of protein accumulated. Our goal in this study was to identify the common steps in the process of cardiac hypertrophy. Our working hypothesis was that in all forms of cardiac hypertrophy glucose utilization increases and that the percentage of energy derived from fatty-acid oxidation decreases. The first part of this study entailed the development and characterization of a neonatal rat heart cell model. The model had to provide uniform culture conditions for rapid development of hypertrophy by agents acting at different sites in the cardiomyocytes. The second part of this study was composed of an assessment of hypertrophy caused by four pharmacologically distinct agents: norepinephrine, angiotensin-II, endothelin-I and tetradecylglycidic acid. In this part we compared the quantity of protein accumulation and quality of hypertrophy cause by each agent. This task was accomplished by examining the effect of each agent on selected mRNA messages and alteration in DNA content of cardiomyocytes. Here we also examined the effect of protein kinase-C, endothelin-I and angiotensin-II inhibitors on hypertrophy caused by each agent. In the final part of this study, metabolic alteration in hypertrophy caused by each agent was assessed for a potential common pathway to hypertrophy. As part of this analysis, we examined changes in glucose and palmitate oxidation, glucose uptake and role of pentose pathway in hypertrophy resulting from treatment of cardiomyocyte by each agent.en_US
dc.typetexten_US
dc.typeDissertation-Reproduction (electronic)en_US
dc.subjectHealth Sciences, Toxicology.en_US
dc.subjectHealth Sciences, Pharmacology.en_US
dc.subjectBiology, Animal Physiology.en_US
dc.subjectHealth Sciences, Pathology.en_US
thesis.degree.namePh.D.en_US
thesis.degree.leveldoctoralen_US
thesis.degree.disciplineGraduate Collegeen_US
thesis.degree.disciplinePharmacology and Toxicologyen_US
thesis.degree.grantorUniversity of Arizonaen_US
dc.contributor.advisorDavis, Thomas P.en_US
dc.identifier.proquest9806843en_US
dc.identifier.bibrecord.b37557300en_US
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