Українська Русский English

ISSN 2522-9028 (Print)
ISSN 2522-9036 (Online)
DOI: https://doi.org/10.15407/fz

Fiziologichnyi Zhurnal

is a scientific journal issued by the

Bogomoletz Institute of Physiology
National Academy of Sciences of Ukraine

Editor-in-chief: V.F. Sagach

The journal was founded in 1955 as
1955 – 1977 "Fiziolohichnyi zhurnal" (ISSN 0015 – 3311)
1978 – 1993 "Fiziologicheskii zhurnal" (ISSN 0201 – 8489)
1994 – 2016 "Fiziolohichnyi zhurnal" (ISSN 0201 – 8489)
2017 – "Fiziolohichnyi zhurnal" (ISSN 2522-9028)

Fiziol. Zh. 2000; 46(6): 84-89


Effect of blockers of sarcolemmal iontransportingsystems on intensivity of heart dammage duringcalcium paradox

V. V. Alabovsky, Cragoe E. J., Jr., A. A. Winokurov

    Department of Biochemistry of Medical Academy, Voronezh, Russia


Abstract

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 depent 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.

References

  1. Baumgarten C. M., Duncan S. W. N. Heart: function and metabolism/Ed. N. S.Dhalla, G. Pierce, R. Beamish.- N.-Y. — 1987. — P. 117-131.
  2. Boron W. F., McCormick W. C., Roos A. pH regulation in barnacle muscle musclefibres: dependence on extracellular sodium and bicarbonate // Amer. J.Physiol. —1981. — 240. — P. C80-C89.
  3. Busselen P. Effect of sodium on calcium paradox in rat hearts // Europ.J.Physiol.(Pfluger’s Arch.) — 1987. — 408. — P. 458-464.
  4. Cala P. M. , Grinstein S. Na/H exchange / Ed. S. Grinstein. — Fl.: CRC, 1988. —P.201-208.
  5. Chapman R. A., Tunstall J. The calcium paradox of the heart // Prog. Biophys. Mol.Biol. — 1987. — 50. — P. 67-96.
  6. Davis B. A., Hogan E. M., Boron W. F. Role of G- proteins in the stimulation of Na-Hexchange by cell shrinkage //Amer. J.Physiol. — 1992. — 262. — P. C533-C536.
  7. Hoffman E. K., Simonsen L. O. Menbrane mechanisms in volume and pH regulation invertebrate cells // Physiol. Rev. — 1989. — 69. — P. 315-382.
  8. Kleyman T .R., Cragoe E. J. Methods in Enzymol. Biomembranes: Biological transportcellular and subcellular. — N.-Y., 1990. — 191. — P. 739-755.
  9. 9. Liu S. , Piwnica-Worms D., Lieberman M. Intracellular pH regulation in culturedembryonic chick heart cells. Na- dependent Cl-HCO3 exchange // J.Gen. Physiol. —1990. — 96. — P. 1247-1269.
  10. 10. Omachi A., Kleps R., Henderson T. O., Labotka R. J. Inhibition of calcium paradox inisoolated rat hearts by high perfusate sucrose concentrations // Amer. J.Physiol. —1994. — 266. — P. H1729-H1737.
  11. Pena-Rasgado C., McGruder K. D., Summers J. C., Rasgado-Flores H. Effect ofisosmotic removal of extracellular Ca2+ and membrane potential on cell volume inmuscle cells // Amer. J.Physiol. — 1994. — 267. — P. C768-C775.
  12. Russel J. M., Boron W. F., Brodwick M. S. Intracellular pH and Na fluxes in barnaclemuscle with evidence for reversal of the ionic mechanism of intracellular pH regulation// J.Gen.Physiol. — 1983. — 82. — P. 47-78.
  13. Sarkadi B., Parker J.C. Activation of ion transport pathways by changes in cell volume// Biochim. Biophys. Acta. — 1991. — 1071. — P. 407-427.
  14. Sheu S.-S., Blaustein M. P. The Heart and Cardiovascular System / Ed. H.A.Fozzard.—N.-Y, 1992. — P. 903-943.
  15. Sorota S. Swelling- induced chloride — sensitive current in canine atrial cells revealedby whole-cell patch- clamp method // Circulet. Res. — 1992. — 70. — P. 679-687.
  16. Tunstall J., Busselen P., Rodrigo G. C., Chapman R. A. Pathways for movements ofions during calcium — free perfusion and the induction of calcium paradox // J. Mol.Cell. Cardiol. — 1986. — 18. — P. 241-254.
  17. Zhang J., Rasmusson R. L., Hall S., Lieberman M. A chloride current associated withswelling of cultured chick heart cells // J.Physiol. — 1993. — 472. — P. 801-820.

© National Academy of Sciences of Ukraine, Bogomoletz Institute of Physiology, 2014-2018.