| Affiliations: | Michael E. DeBakey Institute Undergraduate Research Program |
| Project Leader: | Wesley Fuertes wfuertes@tamu.edu Biomedical Sciences |
| Faculty Mentor: | Randolph Stewart, DVM, Ph.D. |
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Meeting Times:
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Spring 2017: Wed. 10:30 AM-12:00 PM, Thur. 12:45-2:15 PM |
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Team Size:
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3 (Team Full) |
| Open Spots: | 0 |
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Special Opportunities:
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You will gain valuable research experience and chances of earning co-authorship, and we are presenting our findings at the Experimental Biology Conference in April. Also research is a great way of procuring letters of recommendation. |
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Team Needs:
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Experience is not required to join the project. We are looking for enthusiastic students that are able to think creatively. Meeting Times are flexible, you don’t have to be there for the entire time, but it is preferred that you can make the meeting times. |
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Description:
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The twin fields of cardiovascular physiology and cardiac mechanobiology have typically studied independently/ On one hand, cardiovascular physiologists are interested in how ventricular stroke volumes and blood pressures emerge from the complex interaction of the heart and the vasculature. Cardiac contractility, characterized by the slope of the end-systolic pressure-volume relationship, is only one of many factors determining ventricular pressure and stroke volume. The result of cardiac adaptation is characterized by changes in contractility. On the other hand, cardiac mechanobiologists are interested in how tissue stresses result in structural remodeling. Ventricular pressures and volumes are viewed only as boundary conditions that affect wall stress. The stimulus for cardiac adaptation is wall stress. The need to integrate these two fields becomes clear when considering that wall stress affects contractility, and changes in contractility in turn, affects wall stress. Using a simple closed loop model and a simple assumed ventricular geometry, we integrate these two approaches. First, wall stress is found to be a bimodal function of contractility. Second, we make the common assumption that contractility adapts so that it increases with wall stress. These two functions, representing the fundamental assumptions of cardiovascular physiology and cardiovascular mechanobiology, result in a simple balance point that predicts equilibrium contractility. The purpose of the present project therefore is to use the insight arising from mathematical modeling to explore cardiac adaptation in health and disease. |