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用常规细胞内微电极记录绵羊心室浦肯野纤维及肌小梁、和豚鼠心室乳头肌的跨膜动作电位。α-受体激动剂新福林使这三种心肌的动作电位时程(APD)延长。α_2-受体阻断剂育亨宾不能阻断这效应;α_1-受体阻断剂哌唑嗪可阻断这效应。实验中,β-受体阻断剂心得安浓度为1.0×10~(-6)mol/L。实验结果表明,α_1-受体激动可使这三种心肌ADP延长。秩和法统计检验表明。α_1-受体激动对浦肯野纤维APD的延长作用大于对心室肌APD的延长作用;对两种心室肌APD延长作用无显著差异。这提示,特殊传导系统心肌与工作心肌对心肌α_1-受体激动的反应机制有所不同。
The transcellular membrane potential of sheep ventricular Purkinje fibers and trabecular meshwork, and guinea pig ventricular papillary muscles were recorded by conventional intracellular microelectrodes. The neureparin, an a-agonist, prolonged the action potential duration (APD) of all three myocardium. α_2-receptor blocker yohimbine can not block this effect; α_1-receptor blocker prazosin can block this effect. Experiments, β-blocker propranolol concentration of 1.0 × 10 -6 mol / L. The experimental results show that, α_1-receptor activation can extend these three kinds of myocardial ADP. Rank sum method test shows. α 1 -receptor agonist on Purkinje fiber APD prolongation is greater than the ventricular APD prolonging effect on the two ventricular APD extension effect no significant difference. This suggests that there is a difference in the mechanism by which cardiac and working myocardium of a particular conduction system respond to cardiac [alpha] 1 -receptor agonism.