Saxon M E, Filippov A K, Porotikov U I
Basic Res Cardiol. 1984 Nov-Dec;79(6):668-78. doi: 10.1007/BF01908384.
The mechanism of spontaneous diastolic depolarizations induced by different Ca2+ overloading conditions (ouabain toxicity, calcium ionophore A23187, O-K, high Ca2+ solution) in mammalian working myocardium fibres was studied with conventional microelectrode technique and pharmacological approach. Antagonistic properties of antiphospholipase-A2 (PL A2)-active compounds (dexamethasone and indomethacin) were tested. Membrane oscillations in Ca2+ overload conditions were shown to be eliminated or largely protected by both anti-inflammatory agents. There was no influence of the compounds on electrical parameters and ion currents in intact mammalian and amphibian myocardium. The data obtained suggested that modulation of Ca2+-dependent PL A2 activity may contribute significantly to membrane destabilization due to Ca2+ overload of cardiac cells. An analogous membrane destabilizing action of exogenous PL A2 observed in Langendorff-perfused guinea pig heart is in favour of the hypothesis introduced.
采用传统微电极技术和药理学方法，研究了不同钙超载条件（哇巴因毒性、钙离子载体A23187、O-K、高钙溶液）诱导的哺乳动物工作心肌纤维自发性舒张期去极化的机制。测试了抗磷脂酶A2（PL A2）活性化合物（地塞米松和吲哚美辛）的拮抗特性。结果表明，两种抗炎药物均可消除或在很大程度上保护钙超载条件下的膜振荡。这些化合物对完整的哺乳动物和两栖动物心肌的电参数和离子电流没有影响。所获得的数据表明，钙依赖性PL A2活性的调节可能在很大程度上导致由于心肌细胞钙超载引起的膜不稳定。在Langendorff灌注豚鼠心脏中观察到的外源性PL A2类似的膜不稳定作用支持了所提出的假设。
