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Miklós Z, Ivanics T, Roemen TH, et al. Time related changes in calcium handling in the isolated ischemic and reperfused rat heart. Mol Cell Biochem. 2003;250(1):115-24doi: 10.1023/a:1024998200846.
Miklós, Z., Ivanics, T., Roemen, T. H., van der Vusse, G. J., Dézsi, L., Szekeres, M., Kemecsei, P., Tóth, A., Kollai, M., & Ligeti, L. (2003). Time related changes in calcium handling in the isolated ischemic and reperfused rat heart. Molecular and cellular biochemistry, 250(1), 115-24. https://doi.org/10.1023/a:1024998200846
Miklós, Zsuzsa, et al. "Time related changes in calcium handling in the isolated ischemic and reperfused rat heart." Molecular and cellular biochemistry vol. 250,1 (2003): 115-24. doi: https://doi.org/10.1023/a:1024998200846
Miklós Z, Ivanics T, Roemen TH, van der Vusse GJ, Dézsi L, Szekeres M, Kemecsei P, Tóth A, Kollai M, Ligeti L. Time related changes in calcium handling in the isolated ischemic and reperfused rat heart. Mol Cell Biochem. 2003 Aug;250(1):115-24. doi: 10.1023/a:1024998200846. PMID: 12962149.
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Mol Cell Biochem. 2003 Aug;250(1):115-24. doi: 10.1023/a:1024998200846.

Time related changes in calcium handling in the isolated ischemic and reperfused rat heart.

Molecular and cellular biochemistry

Zsuzsa Miklós, Tamás Ivanics, Theo H M Roemen, Ger J van der Vusse, László Dézsi, Mária Szekeres, Péter Kemecsei, András Tóth, Márk Kollai, László Ligeti

Affiliations

  1. Institute of Human Physiology and Clinical Experimental Research, Semmelweis University, Budapest, Hungary.

PMID: 12962149 DOI: 10.1023/a:1024998200846

Abstract

The main aim of this study was to assess the kinetics of intracellular free calcium (Ca(2+)i) handling by isolated rat hearts rendered ischemic for 30 min followed by 30 min of reperfusion analyzing the upstroke and downslope of the Ca(2+)i transient. Changes in mechanical performance and degradation of membrane phospholipids--estimated by tissue arachidonic acid content--were correlated with Ca(2+)i levels of the heart. The fluorescence ratio technique was applied to estimate Ca(2+)i. The disappearance of mechanical activity of the heart preceded that of the Ca(2+)i transient in the first 2 min of ischemia. The slope of upstroke of the Ca(2+)i transient, reflecting Ca2+ release, decreased by 60%, while the duration of the downslope of the transient, reflecting Ca2+ sequestration, expressed a significant prolongation (105 +/- 17 vs. 149 +/- 39 msec) during the first 3 min of ischemia. At about 20 min of ischemia end-diastolic pressure expressed a 3.5-fold increase (contracture) when the fluorescence ratio showed a 2-fold elevation. Reperfusion was accompanied with a further precipitous increase in end-diastolic pressure, while resting Ca(2+)i remained at end-ischemic levels. Increases in the arachidonic acid (AA) content of the ischemic and postischemic hearts were proportional to Ca(2+)i levels. In summary, the present findings indicate that both calcium release and removal are hampered during the early phase of ischemia. Moreover, a critical level of Ca(2+)i and a critical duration of ischemia may exist to provoke contracture of the heart. Upon reperfusion the hearts show membrane phospholipid degradation and signs of stunning exemplified by elevated AA levels, partial recovery of Ca(2+)i handling and sustained depression of mechanical performance.

References

  1. Circ Res. 1990 May;66(5):1268-76 - PubMed
  2. Mol Cell Biochem. 1992 Dec 2;118(1):1-14 - PubMed
  3. J Mol Cell Cardiol. 2000 Jul;32(7):1223-38 - PubMed
  4. Circ Res. 1990 Jan;66(1):135-46 - PubMed
  5. Circ Res. 1989 Oct;65(4):1029-44 - PubMed
  6. Am J Physiol. 1998 Nov;275(5 Pt 2):H1652-62 - PubMed
  7. Am J Physiol. 1996 Nov;271(5 Pt 2):H2145-53 - PubMed
  8. Ann N Y Acad Sci. 1998 Sep 16;853:130-48 - PubMed
  9. Annu Rev Physiol. 1995;57:311-32 - PubMed
  10. Cardiovasc Res. 2001 Jul;51(1):108-21 - PubMed
  11. Am J Physiol. 1988 Oct;255(4 Pt 2):H929-36 - PubMed
  12. J Mol Cell Cardiol. 1996 Jul;28(7):1401-13 - PubMed
  13. Am J Physiol. 1998 May;274(5 Pt 2):H1821-7 - PubMed
  14. Circ Res. 1989 Feb;64(2):304-14 - PubMed
  15. Annu Rev Physiol. 1990;52:543-59 - PubMed
  16. Biochemistry. 2000 Mar 21;39(11):2902-11 - PubMed
  17. Biochem Pharmacol. 1999 May 15;57(10):1079-84 - PubMed
  18. Am J Physiol. 1997 Nov;273(5 Pt 2):H2161-9 - PubMed
  19. J Biol Chem. 1997 Mar 14;272(11):7069-77 - PubMed
  20. Circ Res. 1990 May;66(5):1255-67 - PubMed
  21. Physiol Rev. 1992 Oct;72(4):881-940 - PubMed
  22. Mol Cell Biochem. 1998 Aug;185(1-2):205-11 - PubMed
  23. Circ Res. 1992 Sep;71(3):605-13 - PubMed
  24. Prostaglandins Leukot Essent Fatty Acids. 1997 Jul;57(1):85-93 - PubMed
  25. Circ Res. 1995 Jun;76(6):1036-48 - PubMed
  26. J Biol Chem. 1985 Mar 25;260(6):3440-50 - PubMed
  27. Cardiovasc Res. 1983 Aug;17(8):452-8 - PubMed
  28. Circulation. 1988 Oct;78(4):1047-59 - PubMed
  29. Circ Res. 2000 Aug 18;87(4):275-81 - PubMed
  30. Physiol Rev. 1999 Apr;79(2):609-34 - PubMed
  31. Cardiovasc Res. 1995 Apr;29(4):536-42 - PubMed
  32. Mol Cell Biochem. 2001 Oct;226(1-2):119-28 - PubMed
  33. Cardiovasc Res. 1998 Aug;39(2):423-33 - PubMed
  34. Trends Cardiovasc Med. 1999 Nov;9(8):245-9 - PubMed
  35. J Physiol. 1999 Aug 1;518 ( Pt 3):735-44 - PubMed
  36. Biochem Biophys Res Commun. 1990 Aug 31;171(1):102-8 - PubMed
  37. Cardiovasc Res. 2000 Jan 1;45(1):100-6 - PubMed
  38. Circ Res. 1996 Dec;79(6):1100-9 - PubMed
  39. Am Heart J. 1999 Aug;138(2 Pt 2):S69-75 - PubMed
  40. J Physiol. 1994 Oct 1;480 ( Pt 1):45-60 - PubMed
  41. Circulation. 1989 Dec;80(6 Suppl):IV17-22 - PubMed

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