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- W2137861587 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 + 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 42 K + to measure unidirectional K + efflux rate (in 42 K - washout experiments) or tissue K + content (in 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 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." @default.
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- W2137861587 date "1998-03-01" @default.
- W2137861587 modified "2023-10-14" @default.
- W2137861587 title "Lysophosphatidylcholine and Cellular Potassium Loss in Isolated Rabbit Ventricle" @default.
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- W2137861587 doi "https://doi.org/10.1177/107424849800300105" @default.
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