Ca2+ Transients in Perfused Hearts: Fundamental Properties of the Chemical Signals Underlying Ventricular Mechanics
An increase in the intracellular free calcium concentration, [Ca2+]i, initiates contractile activation in the heart. Until recently, the changes in [Ca2+]i during the cardiac cycle (the “Ca2+ transients”) had eluded measurement. Here I describe the use of gated nuclear magnetic resonance (NMR) spectroscopy to achieve direct quantitation of the cyclical changes in [Ca2+]i that underlie mechanics in perfused ferret hearts loaded with-the fluorinated Ca2+ indicator 5F-BAPTA. [Ca2+]i increased from approximately 200 nM in diastole to 750 nM or higher in early systole. In this preparation, the effects of changing coronary arterial flow on [Ca2+]i can be investigated simultaneously with measurements of high-energy phosphate concentrations by 31P-NMR. When hypoperfusion is induced such that the pressure generated by contraction falls without metabolic evidence of ischemia (“Gregg’s phenomenon”), a decrease in the amplitude of Ca2+ transients underlies the observed fall in pressure. This down-regulation of Ca2+ transients constitutes the cellular basis for Gregg’s phenomenon, and serves to decrease energy demand during low-flow ischemia.
KeywordsCardiac Cycle Nuclear Magnetic Resonance Spectrum Coronary Perfusion Perfuse Heart Early Systole
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