DOI
https://doi.org/10.25772/EBPS-HN83
Defense Date
2017
Document Type
Thesis
Degree Name
Master of Science
Department
Physiology and Biophysics
First Advisor
Dr. Roland Pittman
Abstract
Human essential hypertension affects over 75 million people in the United States, and can lead to death due to its several serious health complications such as hypertension-related cardiovascular disease. The purpose of this research was to understand how hypertension could cause physiological changes to the microcirculation, specifically the PO2 dependence of oxygen consumption (VO2) in skeletal muscle of normotensive and hypertensive rats. The Spontaneously Hypertensive Rat (SHR) strain was used as the diseased model, and Wistar-Kyoto (WKY) rats were used as controls to conduct this study. The SHR strain develops hypertension between 5-6 weeks after birth with an average systolic blood pressure of 150 mmHg. By arresting blood flow using an objective-mounted inflatable airbag, PO2 measurements were obtained along with an oxygen disappearance curve (ODC), which was used to calculate VO2 over various ranges of physiological PO2 values. PO2 and VO2 curves were analyzed based on Hill’s equation to fit the data and describe the PO2 dependence of VO2. When compared to the healthy Wistar-Kyoto rats, the SHRs exhibited a higher Vmax, or maximum rate of oxygen consumption. The average maximal rate of consumption by the hypertensive animal models could be a consequence of a “mitochondrial uncoupling” or some disconnect in the mitochondrial oxygen consumption and the normal corresponding ATP production. In conclusion, this project demonstrated that in situ muscle tissue from hypertensive and normotensive rats had a PO2 dependence of oxygen consumption over a wide range of physiological PO2 values and the hypertensive rats consumed oxygen at a higher maximal rate.
Rights
© The Author
Is Part Of
VCU University Archives
Is Part Of
VCU Theses and Dissertations
Date of Submission
8-4-2017
Included in
Alternative and Complementary Medicine Commons, Cellular and Molecular Physiology Commons, Laboratory and Basic Science Research Commons