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目的:研究双苯氟嗪(DiP)对哇巴因和高钙诱发豚鼠乳头肌迟后除极(DADs)和触发活动(TA)的影响.方法:应用哇巴因(1 μmol/L)和高钙(5.4 mmol/L)诱发稳定且可重复的迟后除极和触发活动.用细胞内玻璃微电极技术记录DADs和TA诸参数.结果:(1)预先应用DiP(10,30 μmol/L)对DADs和TA有明显的抑制作用.在DiP(30 μmol/L)作用下,DADs的幅度由(10.5±2.2)降到(3.6±0.3)mV,DADs时程由(230±19)缩短到(152±14)ms,引起DADs的时间从(21±5)延长至(66±11)min,TA未见发生.(2)诱发DADs后再给予Dip(10,30μmol/L),DADs和TA被明显抑制.在Dip(30μmol/L)作用下,DADS的幅度由(10.4±1.2)降至(3.3±0.6)mV,DADs的时程由(218±22)缩短至(159±26)ms,TA未见发生.结论:Dip对哇巴因和高钙诱发的豚鼠乳头肌迟后除极和触发活动有抑制作用,这可能与其抑制L-型钙通道和/或肌浆网钙释放从而减轻细胞内钙超载有关,并由此产生抗心律失常作用.
Objective: To study the effects of dipfluzine (DiP) on delayed depigmentation (DADs) and triggering activities (TA) in guinea pig papillary muscles induced by ouabain and high calcium.Methods: High calcium (5.4 mmol / L) induces stable and reproducible late depolarization and triggering activities. Intracellular glass microelectrode technique was used to record DADs and TA parameters.Results: (1) Pretreatment with DiP (10,30 μmol / L) significantly inhibited DADs and TA.DAPs amplitude decreased from (10.5 ± 2.2) to (3.6 ± 0.3) mV under DOP (30 μmol / L) (152 ± 14) ms, the duration of DADs prolonged from (21 ± 5) to (66 ± 11) min, but no TA occurred. (2) After DADs were induced, Dip (10,30μmol / DADs and TA were significantly inhibited.The amplitude of DADS decreased from (10.4 ± 1.2) to (3.3 ± 0.6) mV and the duration of DADs decreased from (218 ± 22) to (159 ± 26) ms, TA was not observed.Conclusion: Dip can inhibit the delayed depolarization and triggering activity of guinea pig papillary muscles induced by ouabain and high calcium, which may be related with its inhibition of L-type calcium channel and / or sarcoplasmic reticulum Calcium release thus relieves intracellular calcium overload, and thus produces anti-arrhythmic effects.