Myocardial stunning is associated with impaired calcium uptake by sarcoplasmic reticulum

Sanjay Kumar, Roger J C Hall, Ali R. Mani, Kevin P. Moore, Paolo G. Camici, Ornella E. Rimoldi, Alan J. Williams, Kenneth T. Macleod

Research output: Contribution to journalArticlepeer-review


Myocardial stunning (temporary post-ischaemic contractile dysfunction) may be caused by oxidative stress and/or impaired myocyte calcium homeostasis. Regional myocardial stunning was induced in open-chest pigs (segment shortening reduced to 68.3 ± 4.7% of baseline) by repetitive brief circumflex coronary occlusion (I/R). Reduced glutathione was depleted in stunned myocardium (1.34 ± 0.06 vs. 1.77 ± 0.11 nmol/mg, p = 0.02 vs. remote myocardium) indicating regional oxidant stress, but no regional differences were observed in protein-bound 3-nitrotyrosine or S-nitrosothiol content. Repetitive I/R did not affect myocardial quantities of the sarcolemmal sodium-calcium exchanger, L-type channel, SR calcium ATPase and phospholamban, or the kinetics of ligand binding to L-type channels and SR calcium release channels. However, initial rates of oxalate-supported 45Ca uptake by SR were impaired in stunned myocardium (41.3 ± 13.5 vs. 73.0 ± 15.6 nmol/min/mg protein, p = 0.03). The ability of SR calcium ATPase to sequester cytosolic calcium is impaired in stunned myocardium. This is a potential mechanism underlying contractile dysfunction.

Original languageEnglish
Pages (from-to)77-82
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number1
Publication statusPublished - Sep 11 2009


  • Calcium
  • Ischaemia
  • Myocardial stunning
  • Reactive nitrogen species
  • Reperfusion
  • Sarcoplasmic reticulum

ASJC Scopus subject areas

  • Biochemistry
  • Biophysics
  • Cell Biology
  • Molecular Biology


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