Adenosine prevents cardioplegia-induced Ca2+ loading in cardiac cells

A. Jovanovic, A. Alexeey, J. López, W. Shen, A. Terzic

Research output: Contribution to journalArticlepeer-review


Hyperkalemic cardioplegia is used to arrest the heart during open heart surgery by depolarizing the sarcolemma. A recognized adverse effect of hyperkalemic cardioplegia is ventricular dysfunction related to intracellular Ca2+ loading, but no effective means of protection under these conditions have been established. Whether adenosine, a known cardioprotective agent, could prevent intracellular Ca2+ loading without altering cardioplegia-induced depolarization was investigated using epifluorescent and laser confocal microscopy, and perforated patch-clamp electrophysiology. In ventricular myocytes isolated from guinea pig hearts, and loaded with a Ca2+-sensitive fluorescent probe, exposure of myocytes to 16 mM K+ induced intracellular Ca2+ loading, and membrane depolarization. Yet, adenosine (1 mM) effectively prevented Ca2+ loading whithout reducing the magnitude of cardioplegia-induced depolarization. The preventing effect of adenosine on Ca2+ loading was antagonized by inhibitors of protein kinase C. Adenosine did slow the rate of K+-induced membrane depolarization which could be repsonsible for a decrease in net Ca2+ influx. The property of adenosine to prevent hyperkalemia-induced Ca2+ loading may contribute to the cytoprotective efficacy of this agent as an adjunct to conventional hyperkalemic cardioplegia used in cardiac surgery.

Original languageEnglish (US)
Number of pages1
JournalClinical pharmacology and therapeutics
Issue number2
StatePublished - Dec 1 1997

ASJC Scopus subject areas

  • Pharmacology
  • Pharmacology (medical)


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