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目的 由吡那地尔诱导犬右心室肌细胞产生“全或无”复极,观察奎尼丁对这种跨壁复极离散的影响。方法 应用标准玻璃微电极技术在1000ms刺激周长下,记录犬右心室肌细胞不同部位(外膜下、M区、内膜下)在不同情况[正常对照、吡那地尔(2 5μmol/L)、吡那地尔( 2 5μmol/L) +奎尼丁(5μmol/L) ]的动作电位。结果 吡那地尔( 2 5μmol/L)在3层细胞产生“全或无”复极,使跨壁复极离散增大,动作电位时程跨壁复极离散由(48 .5±9 .2)ms升为(128. 7±13. 5)ms(P<0. 01),进一步灌注奎尼丁(5μmol/L)后,减为(54 .3±10 .8)ms(P<0. 01)。奎尼丁部分恢复动作电位2相平台,延长了被吡那地尔缩短的动作电位时程。结论 在犬右心室肌组织,奎尼丁(5μmol/L)减小了由吡那地尔造成的跨壁复极离散,维持了跨壁电稳定性。
Objectives Pinacidil induces “all or nothing” repolarization in canine right ventricular myocytes, and investigates the effect of quinidine on this transmural repolarization dispersion. Methods Standard glass microelectrode technique was used to record different regions of right canine ventricular myocytes (subepithelial, subterraneal, submandibular) under different circumstance of 1000ms [normal control, pinacidil (25μmol / L ), Pinacidil (25μmol / L) + quinidine (5μmol / L)]. Results Pinacidil (25μmol / L) produced “all or nothing” repolarization in the third layer of cells, which increased the transmural repolarization dispersion and the transmural repolarization discrepancy of action potentials was (48.5 ± 9. (128.7 ± 13.5) ms (P <0.01), and then decreased to (54.3 ± 10.8) ms after further perfusion of quinidine (P <0.05) 0.01). Quinidine partially restored the action potential 2-phase platform, prolonging the shortened action potential duration by pinacidil. Conclusions Quinidine (5 μmol / L) reduced the transmural repolarization dispersion caused by pinacidil and maintained the transmural stability in canine right ventricular muscle.