The heart is a complex organic engine that converts chemical energy into work. Each heartbeat begins with an electrically-released pulse of calcium, which triggers force development and cell shortening, at the cost of energy and oxygen, and the dissipation of heat. My group have developed new instrumentation systems to measure all of these processes simultaneously, while subjecting isolated samples of heart tissue to realistic contraction patterns that mimic the pressure-volume-time loops experienced by the heart with each beat. These devices are effectively 'dynamometers' for the heart, that allow us to measure the performance of the heart and its tissues, much in the same way that you might test the performance of your motor vehicle on a 'dyno.'
This demanding undertaking has required us to develop our own actuators, force transducers, heat sensors, and optical measurement systems. Our instruments make use of several different measurement modalities which are integrated in a robotic hardware-based real-time acquisition and control environment and interpreted with the aid of a computational model. In this way, we can now resolve (to within a few nanoWatts) the heat released by living cardiac muscle fibers as they perform work at 37 °C.
Muscle force and length are controlled and measured to microNewton and nanometer precision by a laser interferometer, while the muscle is scanned in the view of an optical microscope equipped with a fluorescent calcium imaging system. Concurrently, the changing muscle geometry is monitored in 4D by a custom-built optical coherence tomograph, and the spacing of muscle-proteins is imaged in real-time by transmission-microscopy and laser diffraction systems. Oxygen consumption is measured using fluorescence-quenching techniques.
Equipped with these unique capabilities, we have probed the mechano-energetics of failing hearts from rats with diabetes. We have found that the peak stress and peak mechanical efficiency of tissues from these hearts was normal, despite prolonged twitch duration. We have thus shown that the compromised mechanical performance of the diabetic heart arises from a reduced period of diastolic filling and does not reflect either diminished mechanical performance or diminished efficiency of its tissues. In another program of research, we have demonstrated that despite claims to the contrary, dietary supplementation by fish-oils has no effect on heart muscle efficiency. Neither of these insights were fully revealed until the development of this instrument.