Dr. Bailey's Research Lab

I am a cardiac physiologist with interests stemming from the organ level (the whole heart) to the cellular (the individual muscle cells), and beyond (sub-cellular organelles, contractile apparatus, etc.). Since heart disease is a major killer in our country, I (along with lots of others!) am interested in learning more about why the heart works as it does, and why it stops working effectively under certain stresses. In addition, because epidemiological evidence indicates that premenopausal females exhibit a significantly lower risk of heart disease than do age-matched males, we are studying differences in cardiac function between males and females. Finally, one of the stresses that female hearts undergo is the volume stress associated with pregnancy. We have recently begun to study the cardiac hypertrophy that occurs during pregnancy.

The students in my laboratory are currently testing the following interrelated hypotheses:

  1. Basic cardiac function differs between males and females.
  2. Male and female hearts respond differently to calcium stress. Calcium is necessary for cardiac contraction, but too much calcium can cause damage during ischemia-reperfusion injury. Different calcium-handling capabilities between male and female hearts could help explain differences in ischemia-reperfusion injury.
  3. The cardiac hypertrophy that accompanies pregnancy differs from the volume-overload hypertrophy seen in response to chronic exercise. 

We use a mouse model to give us insights into human differences. We study cardiac function at the cellular level by isolating individual cardiac muscle cells (myocytes) from the mouse heart. We use a calcium-sensitive fluorescent dye to measure intracellular calcium while simultaneously measuring sarcomere shortening in electrically-stimulated myocytes to study functional differences between male and female hearts. We are also using immunohistochemistry to study the mechanisms of pregnancy-induced cardiac hypertrophy.