The aim of present study was to investigate a role of different anions in calcium paradox development. It is accepted point of view that development of calcium paradox is depend on cation composition and activity of Na/Ca exchange. However, role of anion composition remain unknown. It is not studied role of some aniontransporting systems in development of calcium paradox. Experiments were carried out on isolated Langendorff perfused rat hearts. Hearts were perfused with calcium-containing solution for 15 minutes, calcium-free medium for 10 minutes and reperfused by initial calcium-containing solution with [Ca2+ = 2 mM]. Release of myoglobin was used as a marker of membrane damage. It has been shown that addition of 5-20 mM HCO3 exacerbated calcium paradox of the heart, elevated myoglobin release from 4.92 +/- 0.57 mcg/g dry weight to 11.3 +/- 1.6 mcg/g dry weight. An inhibitor of HCO3/Cl exchange, 10 mcM L-644,711 depressed elevation of myoglobin release to 4.8 +/- 1.05 mcg/g dry weight. An inhibitor of Cl- channels, 5 mcM DIOA caused raising of myoglobin loss to 7.3 +/- 0.8 mcg/g dry weight during calcium paradox. These data show dependence of calcium paradox on anion composition. A possible reason for exacerbation of calcium paradox by HCO3- rich medium could be consistence of HCO3/Cl and Na/Ca exchange. The results discover new perspectives in myocardial protection of calcium overload.