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Alpha1‐Adrenergic Receptor Modulation of Repolarization in Canine Purkinje Fibers

机译:犬浦肯野纤维复极化的α1-肾上腺素能受体调节

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Alpha‐Agonists and Repolarization.Introduction:Alpha‐adrenergic receptor stimulation increases contractility and prolongs repolarization. These effects are modulated by α1‐adrenergic receptor‐mediated inhibition of transsarcolemmal potassium currents.Methods and Results:We used standard microelectrode techniques to study the actions of 4‐aminopyridine (4‐AP), which blocks the transient outward current, Ito, and WAY‐123,398, which blocks the delayed rectifier, Ik, on canine Purkinje fiber action potential prolongation induced by phenylephrine. At a basic cycle length of 1 second, phenylephrine (0.1 to 10 μ) dose‐dependently prolonged action potential duration at 90 repolarization (APD90) from 331 ± 10 msec to 400 ± 12 msec (P<0.05) at phenylephrine, 10 μ. Phenylephrine did not change phase 1 or plateau height. 4‐AP (0.1 mM) decreased phase 1 magnitude, shifted plateau height to more positive potentials (from 0.1 ± 1.8 mV to 14.3 ± 1.1 mV P<0.05), and shortened APD90from 318 ± 9 msec to 294 ± 8 msec (P<0.05). 4‐AP did not block phenylephrine effects on APD90, which increased, at 10 μ phenylephrine, from 294 ± 8 msec to 342 ± 6 msec (P<0.05). In contrast, WAY‐123,398 (0.1 μ) prolonged APD90from 360 ± 6 msec to 452 ± 6 msec (P<0.05), and had no effect on plateau height. In the presence of WAY‐123,398, phenylephrine no longer increased APD9o.Conclusion:(1) Agents that block Itoshorten APD in Purkinje fibers; and (2) the α‐agonist mediated increase of APD in canine Purkinje fi
机译:简介:α-肾上腺素能受体刺激可增加收缩力并延长复极化。这些作用通过α1-肾上腺素能受体介导的经肌瘤钾电流抑制来调节。方法和结果:我们使用标准微电极技术研究了阻断瞬态向外电流的 4-氨基吡啶 (4-AP) 和 阻断延迟整流器 Ik 的 WAY-123,398 对去氧肾上腺素诱导的犬浦肯野纤维动作电位延长的作用。在 1 秒的基本循环长度下,去氧肾上腺素(0.1 至 10 μ)剂量依赖性地将 90% 复极化 (APD90) 时的动作电位持续时间从 331 ± 10 毫秒延长至 400 ± 12 毫秒 (P<0.05) 在去氧肾上腺素 10 μ。去氧肾上腺素没有改变第 1 阶段或平台高度。4‐AP (0.1 mM) 降低了相位 1 的幅度,将平台高度转移到更正的电位(从 0.1 ± 1.8 mV 到 14.3 ± 1.1 mV [P<0.05]),并将 APD90 从 318 ± 9 毫秒缩短到294 ± 8 毫秒 (P<0.05)。4‐AP没有阻断去氧肾上腺素对APD90的影响,在去氧肾上腺素10 μ时,去氧肾上腺素从294±8毫秒增加到342±6毫秒(P<0.05)。相比之下,WAY-123,398 (0.1 μ) 将 APD90 从 360 ± 6 毫秒延长至 452 ± 6 毫秒 (P<0.05),对平台高度没有影响。在WAY-123,398存在下,去氧肾上腺素不再增加APD9o.结论:(1)阻断Ito缩短浦肯野纤维中APD的药物;(2)α激动剂介导的犬浦肯野犬APD增加

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