Background:
The effect of a metabolic change on excitation-contraction (EC) coupling is poorly understood in the atrial myocardium, while the previous studies have mainly focused on EC coupling in the ventricular myocardioum. Although the myocardium mostly uses fatty acid as an energy source, we have reported that metabolic substrate, includes lactate, can be used for energy production and that the metabolomic profile is different between the atria and the ventricles in mouse heart. In addition, it is still under discussion whether lactate can be an energy source for muscles. In the present study, we aimed to investigate the effect of lactate exposure on EC coupling in the atrial and the ventricular myocardium.
Methods:
We micro-injected aequorin (a Ca2+-sensitive photoprotein) into superficial cells of the left atrium and/or the left ventricular papillary muscle isolated from mice (C57/BL6, 12 - 17 weeks of age), and simultaneously measured intracellular Ca2+ concentration and tension (1 Hz at 36 °C). We added lactate (~10 mM) into HEPES-Tyrode solution (pH was adjusted at 7.4) and observed the changes in the peak tension and the peak Ca2+ concentration.
Results and Conclusion:
Lactate at a concentration of 10 mM significantly decreased the peak tension (61.7±6.0%; n = 3; P < 0.05.) and the peak Ca2+ concentration (78.8±4.8%; n = 3; P < 0.05.) in the atrial myocardium. Although we observed similar effect of lactate on the ventricular papillary muscle, it was modest compared with the atrial myocardium (72.8±5.6%, 91.6±13.5%, peak tension and Ca2+, respectively; n = 3; no significance). Our results suggest that the atrium has different characteristic of EC coupling from the ventricles in response to an increase in lactate, of which condition is often observed in myocardial ischemia. Moreover, lactate did not seem to contribute to make energy in terms of the tension in the heart. Simultaneous measurement of tension and intracellular Ca2+ concentration can be useful to analyze the atrial physiological property.