Potassium channel openers prevent potassium-induced calcium loading of cardiac cells: Possible implications in cardioplegia

J. R. Lopez, R. Jahangir, A. Jahangir, W. K. Shen, A. Terzic

Research output: Contribution to journalArticle

66 Citations (Scopus)

Abstract

Hyperkalemic solutions that are used as cardioplegic agents, while effective in inducing electromechanical arrest, are only partially cardioprotective, and ventricular dysfunction has been observed. The underlying pathophysiology of cardioplegia-associated ventricular dysfunction is complex and not fully understood, but it could be related, in part, to intracellular Ca2+ loading induced by high K+ concentrations present in cardioplegic solutions. Yet no effective cytoprotective means against possible intracellular Ca2+ loading, under these conditions, has been described. Recently, potassium channel openers, which open adenosine triphosphate-sensitive K+ channels, have been reported to possess cardioprotective properties under global ischemic conditions. However, it is not known whether these novel agents could prevent intracellular Ca2+ loading that could occur during cardioplegia. Intracellular Ca2+ was monitored in ventricular myocytes, loaded with the Ca2+-sensitive fluorescent probe Fluo-3AM, using epifluorescent digital imaging and laser confocal microscopy. Exposure of a myocyte to a 16 mmol/L concentration of K+, a concentration of K+ commonly used in cardioplegic solutions, induced a nonhomogeneous increase in intracellular Ca2+. Potassium channel opening drugs, such as aprikalim or nicorandil, effectively prevented these solutions from increasing intracellular Ca2+. The preventive effect of potassium channel opening drugs was antagonized by glyburide, a selective blocker of adenosine triphosphate-sensitive K+ channels. This study demonstrates, at the single cardiac cell level, that solutions containing a 16 mmol/L concentration of K+ promote intracellular Ca2+ loading, which can be prevented by potassium channel opening drugs. Therefore, potassium channel opening drugs should be considered to prevent intracellular Ca2+ loading associated with the use of cardioplegic solutions.

Original languageEnglish (US)
Pages (from-to)820-831
Number of pages12
JournalJournal of Thoracic and Cardiovascular Surgery
Volume112
Issue number3
DOIs
StatePublished - 1996
Externally publishedYes

Fingerprint

Induced Heart Arrest
Potassium Channels
Cardioplegic Solutions
Potassium
Calcium
Ventricular Dysfunction
Confocal Microscopy
Pharmaceutical Preparations
Muscle Cells
Adenosine Triphosphate
Nicorandil
Glyburide
Fluorescent Dyes

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine
  • Surgery

Cite this

Potassium channel openers prevent potassium-induced calcium loading of cardiac cells : Possible implications in cardioplegia. / Lopez, J. R.; Jahangir, R.; Jahangir, A.; Shen, W. K.; Terzic, A.

In: Journal of Thoracic and Cardiovascular Surgery, Vol. 112, No. 3, 1996, p. 820-831.

Research output: Contribution to journalArticle

Lopez, J. R. ; Jahangir, R. ; Jahangir, A. ; Shen, W. K. ; Terzic, A. / Potassium channel openers prevent potassium-induced calcium loading of cardiac cells : Possible implications in cardioplegia. In: Journal of Thoracic and Cardiovascular Surgery. 1996 ; Vol. 112, No. 3. pp. 820-831.
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