α_1受体激动对浦肯野纤维延迟后除极的双相效应

Biphasic Effects of α_1-Adrenoceptor Activation on the Delayed After Depolarization in Sheep Cardiac Purkinje Fibers

用乙酰毒毛旋花子甙元（ＡＳ）２×１０－７ｍｏｌ／Ｌ中毒诱发绵羊心室浦肯野纤维产生延迟后除极（ＤＡＤ）作为模型，在心得安５×１０－７ｍｏｌ／Ｌ作用下观察苯肾上腺素（ＰＥ）１０－７ｍｏｌ／Ｌ、３×１０－７ｍｏｌ／Ｌ和１０－６ｍｏｌ／Ｌ等不同浓度对ＤＡＤ幅值的影响。６０ｍｉｎ持续灌流中，前２０ｍｉｎＤＡＤ幅值分别增加８％、９％和１０％（每一浓度ｎ＝８，Ｐ＜０．０５）；随后４０ｍｉｎ内，ＤＡＤ幅值呈剂量依赖性减小，ＰＥ１０－７ｍｏｌ／Ｌ减值６．９±０．２％（ｎ＝８，Ｐ＜０．０５），ＰＥ３×１０－７ｍｏｌ／Ｌ减值１３．９±０．１％（ｎ＝８，Ｐ＜０．０１），ＰＥ１０－６ｍｏｌ／Ｌ减值１８．６±０．２％（ｎ＝８，Ｐ＜０．０１）。ＰＥ的作用可被哌唑嗪５×１０－７ｍｏｌ／Ｌ所阻断，提示ＰＥ作用经α１受体兴奋引起。

By using acetyl strophanthidin (AS) 0.2 μmol/L, a stable delayed afterdepolarization (DAD) in sheep cardiac Purkinje fibers was induced as a model. In the presence of propranolol 0.5 μmol/L, effects of phenylephrine(PE) at different concentrations of 0.1, 0.3 and 1.0 μmol/L on the DAD amplitude were observed during a perfusion of 60 min. In the first 20 min, the amplitude of DAD was increased by 8%, 9% and 10% respectively. (n=8, for each dose, P<0.05);20 min later, the increased DAD amplitude gradually declined in a dose dependent manner. The decrease of the amplitude of DAD by PE 0.1 μmol/L was 6.9±0.2% (n=8, P<0.05), by PE 0.3 μmol/L, 13.9±0.1% (n=8, P<0.01)and by PE 1.0 μmol/L, 18.6±0.2% (n=8, P<0.01).The action of PE could be completely blocked by prazosine 0.5 μmol/L. It suggested the effects of PE was via the α1-adrenergic receptor.