Masters Theses

Date of Award

12-1998

Degree Type

Thesis

Degree Name

Master of Science

Major

Engineering Science

Major Professor

Judy L. Cezeaux

Committee Members

John H. Forrester, Richard J. Jendrucko

Abstract

An estimated 58.2 million Americans have one or more types of cardiovascular disease. In addition, cardiovascular disease was responsible for the deaths of almost one million people in the United States alone in 1995. A major risk indicator of cardiovascular disease is left ventricular hypertrophy.

Left ventricular hypertrophy is an adaptive process by the heart that occurs when there is an increase in the mass of the ventricular wall. It is characterized by myocyte hypertrophy and nonmyocyte hyperplasia.

The stimuli responsible for left ventricular hypertrophy are not yet completely understood. Mechanical and humoral factors have been isolated as the main cause of left ventricular hypertrophy. Cardiomyocyte hypertrophy and nonmyocyte hyperplasia increase with mechanical stimuli such as stretch. Products of the renin-angiotensin system have also been shown to stimulate the structural remodeling characteristics of left ventricular hypertrophy including an increase in collagen synthesis which is believed to lead to fibrosis in the interstitial compartment of the heart.

This study examined the relationship between mechanical and humoral stimuli on nonmyocyte proliferation and collagen synthesis. Stretch combined with angiotensin II and/or aldosterone was investigated to see if nonmyocyte hyperplasia was increased or cardiac fibroblast collagen synthesis production elevated. In the proliferation studies, the only condition shown to result in a statistically significant increase in cell number occurred in the case where cells were stretched in the presence of both angiotensin II and aldosterone.

Experiments examining the synthesis of collagen showed an increase in the percent collagen in the stretched cells for all cases, but none of the cases, regardless of hormone condition in the media, showed a statistical significance for increase in the production of collagen.

These results suggest that stretch with a combination of angiotensin II and aldosterone increases nonmyocyte hyperplasia and therefore adds support to the evidence of the renin-angiotensin system's effect on left ventricular hypertrophy. The collagen synthesis study, although there were no statistically significant changes, does appear to indicate an increase due to stretch which supports the theory that collagen production may be elevated in conjunction with productions of the renin-angiotensin and aldosterone system. This increase in collagen may lead to fibrosis in the cardiac interstitium.

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