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KMID : 0880520070430030168
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Chonnam Medical Journal
2007 Volume.43 No. 3 p.168 ~ p.176
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Role of Plasmalogen-derived Lysolipids on the Pathophysiology of Myocardial Ischemia
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Park Ling-Hua
Kim Jae-Ha
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Abstract
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To clarify the role of plasmalogen-derived lysolipids on pathophysiology of myocardial ischemia, effects of the lysolipids on the regulation of ATP-sensitive K+ channel (K(ATP) channel) activities were examined in enzymatically isolated ventricular cardiac myocytes using excised inside-out, cell-attached and whole-cell patch clamp techniques. In the inside-out patches, lysoplasmenylcholine (LPC), in doses ranging from 0.2 to 20micron mol/L, reduced K(ATP) channel activities in a dose-dependent manner. Both the channel opening frequency and the mean open-burst duration were markedly decreased, but the amplitude of the single channel current was not affected. There was no channel activation by the LPC, even when the channel activities had been attenuated by the addition of ATP (100micron mol/L). In cell-attached patches, LPC decreased the dinitrophenol, a metabolic inhibitor, -induced channel activities with the same range of doses as in the inside-out patches. In the whole-cell patches, no channel currents were developed by the LPC itself; however, a K(ATP)-channel opener, PCO400-induced outward currents were attenuated by the LPC (0.2~20micron mol/L). Lysoplasmenylethanolamine (LPE), doses up to 200micron mol/L, did not affect the K(ATP) channel activities in all 3 patch-clamp configurations. From these results, it was inferred that a certain plasmalogen- derived lysolipid is involved in the regulation of ATP-sensitive potassium channel activity in the mouse cardiac myocytes, and that the effects of LPC would be harmful to ischemic myocardium inhibiting K(ATP) channel activities.
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KEYWORD
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Plasmalogen, Lysolipids, Ischemia, K(ATP) channel, Cardiac myocytes
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