Some effects of iproveratril (Isoptin) on the cardiovascular system.
Some effects of iproveratril (Isoptin) on the cardiovascular system.
复制标题
异丙曲（Isoptin）对心血管系统的一些影响。
DOI：
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发表时间：
1968
影响因子：
3.5
通讯作者：
T. E. Lowe
中科院分区：
文献类型：
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作者：
W. Nayler;I. Mcinnes;J. Swann;J. Price;V. Carson;D. Race;T. E. Lowe
采用完整家兔、langendorff灌注大鼠心脏、犬乳头肌和犬心肺搭桥制剂，研究了异丙戊三酯（α-异丙基-α[n -甲基- n -同丙戊基]-γ-氨基丙基-3,4-二甲氧基苯酚乙腈盐酸；异optin； Verpamil）对心血管系统的影响。在正常家兔中，0.1 ~ 0.5 mg/kg的异丙戊三酯引起低血压和心动过缓；异丙肾上腺素输注异丙肾上腺素引起脉压和心率升高，全身血压轻微升高。在离体大鼠心脏中，0.1至0.5µg/ml的异丙肾上腺素抑制和减缓了收缩，但随后添加异丙肾上腺素产生了正的肌力和变时反应，并增加了a型磷酸化酶的百分比，表明没有β肾上腺素能阻断。异丙戊三酯0.05 ~ 03 mg/kg可使移位犬左心室“工作”功能向右弯曲，并对离体乳头肌产生负性肌力作用。这些变化被异丙肾上腺素逆转。在外周循环中，异丙曲利引起血管舒张。异丙肾上腺素在异丙戊三酯存在时不能产生进一步的血管扩张，而eledoisin则可以。依普罗特利持续降低冠状动脉循环中的阻力血流量；它不能阻断星状神经节刺激的心脏作用。这些结果被解释为，异丙戊三酯对心肌的负性肌力和变时作用并不反映β -肾上腺素能阻滞，该药物可能仅在外周循环中产生β -肾上腺素能阻滞。依普罗特利对心血管系统的影响不因先前服用丙素、利血平或β肾上腺素能阻断药物而改变。
The effect of iproveratril (α-isopropyl-α[N-methyl-N-homoveratryl]-γ-aminopropyl-3,4-dimethoxyphenol acetonitrile hydrochloride; Isoptin; Verpamil) on the cardiovascular system was investigated using intact rabbits, Langendorff-perfused rat hearts, dog papillary muscles and dog heart-lung bypass preparations. In intact rabbits 0.1 to 0.5 mg/kg of iproveratril caused hypotension and bradycardia; after iproveratril the infusion of isoproterenol caused an increase in pulse pressure and heart rate, and a slight rise in systemic blood pressure. In isolated rat hearts 0.1 to 0.5 µg/ml of iproveratril depressed and slowed the contractions, but the subsequent addition of isoproterenol produced positive inotropic and chronotropic responses and an increase in the percentage of phosphorylase enzyme in the a form, indicating the absence of beta adrenergic blockade. Iproveratril, 0.05 to 03 mg/kg, displaced dog left ventricular "work" function curves to the right and exerted a negative inotropic effect on isolated papillary muscles. These changes were reversed by isoproterenol. In the peripheral circulation iproveratril caused vasodilation. In the presence of iproveratril isoproterenol failed to produce further vasodilation, whereas eledoisin did so. Iproveratril consistently reduced the resistance blood flow in the coronary circulation; it did not block the cardiac effect of stellate ganglion stimulation. These results are interpreted to mean that the negative inotropic and chronotropic effect of iproveratril on heart muscle does not reflect beta adrenergic blockade and that this drug may produce beta adrenergic blockade in the peripheral circulation only. The effects of iproveratril on the cardiovascular system were not modified by the prior administration of propantheline, reserpine or beta adrenergic blocking drugs.