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Goldhaber JI, Deutsch N, Alexander LD, et al. Lysophosphatidylcholine and Cellular Potassium Loss in Isolated Rabbit Ventricle. J Cardiovasc Pharmacol Ther. 1998;3(1):37-42doi: 10.1177/107424849800300105.
Goldhaber, J. I., Deutsch, N., Alexander, L. D., & Weiss, J. N. (1998). Lysophosphatidylcholine and Cellular Potassium Loss in Isolated Rabbit Ventricle. Journal of cardiovascular pharmacology and therapeutics, 3(1), 37-42. https://doi.org/10.1177/107424849800300105
Goldhaber, et al. "Lysophosphatidylcholine and Cellular Potassium Loss in Isolated Rabbit Ventricle." Journal of cardiovascular pharmacology and therapeutics vol. 3,1 (1998): 37-42. doi: https://doi.org/10.1177/107424849800300105
Goldhaber JI, Deutsch N, Alexander LD, Weiss JN. Lysophosphatidylcholine and Cellular Potassium Loss in Isolated Rabbit Ventricle. J Cardiovasc Pharmacol Ther. 1998 Jan;3(1):37-42. doi: 10.1177/107424849800300105. PMID: 10684479.
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J Cardiovasc Pharmacol Ther. 1998 Jan;3(1):37-42. doi: 10.1177/107424849800300105.

Lysophosphatidylcholine and Cellular Potassium Loss in Isolated Rabbit Ventricle.

Journal of cardiovascular pharmacology and therapeutics

Goldhaber, Deutsch, Alexander, Weiss

Affiliations

  1. Departments of Medicine, University of California Los Angeles School of Medicine, Los Angeles, California, USA

PMID: 10684479 DOI: 10.1177/107424849800300105

Abstract

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(+) accumulation 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 (42)K(+) to measure unidirectional K(+) efflux rate (in (42)K(+) washout experiments) or tissue K(+) content ((42)K(+) 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 tissue 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.

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