With each beat of the heart, its cells release calcium, which triggers force development and shortening, funded by expenditure of energy with its attendant heat liberation and oxygen consumption. We are developing new instruments to monitor all of these processes simultaneously, while subjecting isolated samples of heart tissue to contraction patterns that mimic the pressure-volume-time loops experienced by the heart with each beat. This demanding undertaking has required us to develop our own actuators, force transducers, heat sensors, and optical measurement systems, and to synchronise these in our new measurement device: The Cardiac Myometer.
Our system can resolve the heat released by cardiac trabeculae at 37 °C, to a few nanoWatts1 . Muscle force and length are controlled and measured by a laser interferometer2 , while the muscle is scanned in the view of an optical microscope equipped with a Fura-2 calcium imaging system. Concurrently, trabecula geometry is monitored in 3D by an optical coherence tomograph3 , and sarcomere length distribution is imaged in real-time by transmission-microscopy4 and laser diffraction systems. O¬2 consumption will be measured using fluorescence-quenching techniques.
Equipped with these capabilities, we have probed the mechano-energetics of failing hearts from rats with streptozotocin-induced diabetes. We found that the peak twitch stress and peak mechanical efficiency of diabetic trabeculae from these hearts was normal, despite prolonged twitch duration. We conclude that the compromised mechanical performance of the diabetic heart arises from a reduced period of diastolic filling which, as a consequence of the Frank-Starling mechanism, impairs the following beat - impairment that does not reflect either diminished mechanical performance or diminished efficiency of its tissues5 .