Selective attenuation by adenosine of arrhythmogenic action of isoproterenol on ventricular myocytes.
Selective attenuation by adenosine of arrhythmogenic action of isoproterenol on ventricular myocytes.
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腺苷选择性减弱异丙肾上腺素对心室肌细胞的致心律失常作用。
DOI：
10.1152/ajpheart.2001.280.6.h2789
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发表时间：
2001
期刊：
影响因子：
--
通讯作者：
Belardinelli,L
中科院分区：
文献类型：
--
作者：
Song,Y;Shryock,JC;Knot,HJ;Belardinelli,L
我们研究了腺苷是否同样地减弱了异丙肾上腺素对豚鼠分离的心室肌细胞心律失常活动和收缩缩短的刺激作用。用贴片电极记录跨膜电压和全细胞电流，用视频运动检测器测量细胞收缩。异丙肾上腺素增加动作电位50%复极时程(APD50)、L型钙电流[ICa(L)]、细胞收缩缩短和诱发延迟后除极(DAD)、瞬时内向电流(ITI)和后收缩。腺苷减弱异丙肾上腺素的致心律失常作用大于减弱异丙肾上腺素对APD50、ICA(L)或收缩缩短的影响。腺苷(0.1100Mol/L)使DADS幅度降低30±6%~92±5%，但对异丙肾上腺素引起的APD50延长仅减弱14±4%~59±4%，对动作电位平台电压无影响。腺苷(30μ/L)抑制ITi91±4%，而抑制异丙肾上腺素刺激的ICa(L)仅30±12%。腺苷(10μ/L)可阻断异丙肾上腺素诱发的后收缩，但不降低收缩缩短的幅度。A1-腺苷受体激动剂CPA(N6-环戊基腺苷)和兰尼定可模拟腺苷对收缩缩短和后收缩的影响。综上所述，腺苷可拮抗β肾上腺素能刺激对心肌细胞的致心律失常作用，但不能减少细胞的收缩。
We examined whether adenosine equally attenuated the stimulatory effects of isoproterenol on arrhythmic activity and twitch shortening of guinea pig isolated ventricular myocytes. Transmembrane voltages and whole cell currents were recorded with patch electrodes, and cell twitch shortening was measured using a video-motion detector. Isoproterenol increased the action potential duration at 50% repolarization (APD50), L-type Ca2+current [ICa(L)], and cell twitch shortening and induced delayed afterdepolarizations (DAD), transient inward current (ITi), and aftercontractions. Adenosine attenuated the arrhythmogenic actions of isoproterenol more than it attenuated the effects of isoproterenol on APD50,ICa(L), or twitch shortening. Adenosine (0.1–100 μmol/l) decreased the amplitude of DADs by 30 ± 6% to 92 ± 5% but attenuated isoproterenol-induced prolongation of the APD50by only 14 ± 4% to 59 ± 4% and had no effect on the voltage of action potential plateau. Adenosine (30 μmol/l) inhibitedITiby 91 ± 4% but decreased isoproterenol-stimulatedICa(L)by only 30 ± 12%. Isoproterenol-induced aftercontractions were abolished by adenosine (10 μmol/l), whereas the amplitude of twitch shortening was not reduced. The effects of adenosine on twitch shortenings and aftercontractions were mimicked by the A1-adenosine receptor agonist CPA (N6-cyclopentyladenosine) and by ryanodine. In conclusion, adenosine antagonized the proarrhythmic effect of β-adrenergic stimulation on ventricular myocytes without reducing cell twitch shortening.