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 language||English (US)|
|Number of pages||1|
|Journal||Clinical Pharmacology and Therapeutics|
|State||Published - 1997|
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