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Lysophosphatidylcholine and Cellular Potassium Loss in Isolated Rabbit Ventricle

Department of Medicine, University of California Los Angeles School of Medicine

Nicholas Deutsch

Department of Anesthesiology, University of California Los Angeles School of Medicine, Los Angeles, California

Laura D. Alexander

Department of Medicine, University of California Los Angeles School of Medicine

James N. Weiss

Department of Medicine, University of California Los Angeles School of Medicine, Department of Physiology, University of California Los Angeles School of Medicine

Background: Lysophospholipids such as lysophosphatidylcholine (LPC) have many direct electrophysiological effects on cardiac muscle and have been implicated as a cause of lethal ventricular arrhythmias during acute myocardial ischemia. Because extracellular K ⁺ accu mulation is also a key arrhythmogenic factor during acute ischemia, we examined the effects of LPC on cellular K⁺ balance, including its interaction with adenosine triphosphate- sensitive K+ (K_ATP) channels.

Methods and Results : Isolated rabbit interventricular septa paced at 75 beats/min were loaded with ⁴²K⁺ to measure unidirectional K⁺ efflux rate (in ⁴²K^- washout experiments) or tissue K ⁺ content (in ⁴²K⁺ uptake experiments) and action potential duration (APD) during exposure to 20 µM LPC for 30 minutes. LPC caused tissue K⁺ content to decrease by 15 ± 2% (n = 4) at a steady rate over 30 minutes, associated with gradual APD shortening and a delayed increase in unidirectional K⁺ efflux rate. Pretreatment with 12 µM cromakalim to selectively activate K_ATP channels shortened APD by 44 ± 66% and had no effect on net tis sue K⁺ content during control aerobic perfusion. However, cromakalim increased net K⁺ loss during exposure to LPC to 22 ± 4%, a 47% increase.

Conclusions: LPC induced net K loss in heart, which was potentiated by the K_ATP channel agonist cromakalim. This ATP finding suggests that if LPC accumulates to similar levels during myocardial ischemia and hypoxia, it may be an important mechanism in net K⁺ loss.

Key Words: amphiphiles • ischemia • heart • arrhythmias.

Journal of Cardiovascular Pharmacology and Therapeutics, Vol. 3, No. 1, 37-42 (1998)
DOI: 10.1177/107424849800300105


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