Aniukhovskiĭ E P, Rosen M R
Kardiologiia. 1993;33(9):47-51, 5.
In the present study, the authors used two specific blockers of alpha 1-adrenergic receptor subtypes (chloroethyclonidine and WB-4101) to determine the mechanisms responsible for automatic rhythm occurring during simulated ischemia and reperfusion of isolated canine Purkinje fibers. In the control situation, all fibers showed membrane potentials greater than -90 mV and normal automatic rhythm. During simulated ischemia, the membrane potential depolarized to the -60 mV range. Abnormal automaticity was seen in 20% of fibers untreated with phenylephrine and in 50% of those supervised with 10(-7) M phenylephrine. The incidence of abnormal automaticity was reduced to 0% with WB-4101 and increased to 90% with chloroethylclonidine. Moreover, the ischemic fibers were significantly more hyperpolarized during superfusion with WB-4101 than with chloroethylclonidine. It is concluded that automatic arrhythmias induced by alpha 1-adrenergic stimulation during simulated ischemia may be attributed to a specific alpha 1-adrenergic receptor subtype that is blocked by WB-4101.
在本研究中,作者使用了两种α1 - 肾上腺素能受体亚型的特异性阻滞剂(氯乙可乐定和WB - 4101)来确定在离体犬浦肯野纤维模拟缺血和再灌注期间发生自动节律的机制。在对照情况下,所有纤维的膜电位均大于 - 90mV且具有正常的自动节律。在模拟缺血期间,膜电位去极化至 - 60mV范围。在未用去氧肾上腺素处理的纤维中,20%出现异常自律性,而在用10(-7)M去氧肾上腺素处理的纤维中,50%出现异常自律性。使用WB - 4101时,异常自律性的发生率降至0%,而使用氯乙可乐定时则升至90%。此外,与氯乙可乐定相比,在用WB - 4101灌注期间,缺血纤维的超极化程度明显更高。结论是,模拟缺血期间α1 - 肾上腺素能刺激诱导的自动性心律失常可能归因于一种被WB - 4101阻断的特定α1 - 肾上腺素能受体亚型。