[The role of ion transport system of sarcolemma in amino acid loss during myocardial perfusion with calcium-free medium and myocardium injury during "calcium paradox"].

: The loss of myocardial amino acids is known to depend on sodium gradient across sarcolemma. This is regulated by changes of cellular volume as well. It is suggested that loss of amino acids can be regulated by blocking of anion-transporting systems during Ca-free perfusion. It have been found that calcium depletion from extracellular medium exacerbates release of amino acids two- four fold. Sodium lowering (from 140 mM to 30 mM) accelerates and sodium elevation (from 140 mM to 200 mM) attenuates loss of taurine, glutamine, glycine, glutamate, aspartate, alanine and asparagine, but does not hydrophobic amino acids. Inhibition of CI- channels by IAA94 or K-Cl cotransport with DIOA increases the loss of taurine, glutamine, glycine, glutamate, aspartate, alanine and asparagine during Ca-free perfusion. The release of amino acids during Ca-free perfusion is negatively correlated with recovery of oxidative phosphorylation during the second phase the calcium paradox-Ca-readmission.