RESUMO
Cardiac myocyte sodium (Na+) homoeostasis is pivotal in cardiac diseases and heart failure. Intracellular Na+ ([Na+]i) is an important regulator of excitation-contraction coupling and mitochondrial energetics. In addition, extracellular Na+ ([Na+]e) and its water-free storage trigger collagen cross-linking, myocardial stiffening and impaired cardiac function. Therefore, understanding the allocation of tissue Na+ to intra- and extracellular compartments is crucial in comprehending the pathophysiological processes in cardiac diseases. We extrapolated [Na+]e using a three-compartment model, with tissue Na+ concentration (TSC) measured by in vivo 23Na-MRI, extracellular volume (ECV) data calculated from T1 maps, and [Na+]i measured by in vitro fluorescence microscopy using Na+ binding benzofuran isophthalate (SBFI). To investigate dynamic changes in Na+ compartments, we induced pressure overload (TAC) or myocardial infarction (MI) via LAD ligation in mice. Compared to SHAM mice, TSC was similar after TAC but increased after MI. Both TAC and MI showed significantly higher [Na+]i compared to SHAM (around 130% compared to SHAM). Calculated [Na+]e increased after MI, but not after TAC. Increased TSC after TAC was primarily driven by increased [Na+]i, but the increase after MI by elevations in both [Na+]i and [Na+]e.