Adenosine prevents hyperkalemia-induced calcium loading in cardiac cells

Relevance for cardioplegia

Aleksander Jovanović, Alexey E. Alekseev, Jóse R. López, Win K. Shen, Andre Terzic

Research output: Contribution to journalArticle

40 Citations (Scopus)

Abstract

Background. Hyperkalemic cardioplegic solutions effectively arrest the heart but also induce membrane depolarization, which could lead to intracellular Ca2+ loading and contribute to ventricular dysfunction associated with cardiac operations. Adenosine, which possesses cardioprotective properties, has been proposed as an adjunct to conventional cardioplegic solutions. However, it is not known whether adenosine supplementation enables cardiac cells to withstand hyperkalemia-induced Ca2+ loading. Methods. Single ventricular cardiomyocytes were isolated from guinea pig hearts, loaded with a Ca2+-sensitive fluorescent probe, and imaged by digital epifluorescent microscopy. The emitted fluorescence of the probe, a measure of the intracellular Ca2+ concentration, was recorded from single myocytes during hyperkalemic challenges in the absence and the presence of adenosine to assess the protective effectiveness of this agent. Results. Hyperkalemic solutions induced intracellular Ca2+ loading (estimated intracellular Ca2+ concentration, 88 ± 5 nmol/L before and 1,825 ± 112 nmol/L after addition of 16 mmol/L KCl). Adenosine (1 mmol/L) prevented K+-induced Ca2+ loading (intracellular Ca2+ concentration, 86 ± 6 nmol/L before and 85 ± 8 nmol/L after exposure to K+). Whereas glyburide (3 μmol/L), an antagonist of adenosine triphosphate-sensitive K+ channels, had no effect, staurosporine (200 nmol/L) and chelerythrine (5 μmol/L), two inhibitors of protein kinase C, did abolish the action of adenosine. Conclusions. Adenosine prevents hyperkalemia-induced Ca2+ loading in cardiomyocytes. This effect is due to a direct action on ventricular cells, as the preparation employed was free from atrial, neuronal, and vascular elements, and appears to be mediated through a protein kinase C- dependent mechanism. 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 cardioplegic solutions.

Original languageEnglish (US)
Pages (from-to)153-161
Number of pages9
JournalAnnals of Thoracic Surgery
Volume63
Issue number1
DOIs
StatePublished - Jan 1997
Externally publishedYes

Fingerprint

Induced Heart Arrest
Hyperkalemia
Adenosine
Calcium
Cardioplegic Solutions
Cardiac Myocytes
Protein Kinase C
Ventricular Dysfunction
Protective Agents
Staurosporine
Glyburide
Heart Arrest
Fluorescent Dyes
Muscle Cells
Blood Vessels
Microscopy
Guinea Pigs
Adenosine Triphosphate
Fluorescence
Membranes

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Adenosine prevents hyperkalemia-induced calcium loading in cardiac cells : Relevance for cardioplegia. / Jovanović, Aleksander; Alekseev, Alexey E.; López, Jóse R.; Shen, Win K.; Terzic, Andre.

In: Annals of Thoracic Surgery, Vol. 63, No. 1, 01.1997, p. 153-161.

Research output: Contribution to journalArticle

Jovanović, Aleksander ; Alekseev, Alexey E. ; López, Jóse R. ; Shen, Win K. ; Terzic, Andre. / Adenosine prevents hyperkalemia-induced calcium loading in cardiac cells : Relevance for cardioplegia. In: Annals of Thoracic Surgery. 1997 ; Vol. 63, No. 1. pp. 153-161.
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