维拉帕米和苯氧苄胺对镍致麻醉犬冠状动脉收缩的影响。

A Koller, G Rubányi, L Ligeti, A G Kovách
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引用次数: 0

摘要

我们在狗心脏原位研究了在选择性钙拮抗剂维拉帕米存在下,以及用苯氧苄胺(phenoxybenzamine, PBZ)阻断α受体后,镍诱导的冠状动脉血管收缩。维拉帕米完全消除低剂量Ni2+ (0.02 ~ 0.2 mg/kg-1)对冠状动脉血流量(CBF)和基底电导(BC)的降低作用。维拉帕米逆转了高剂量Ni2+ (2.0-20.0 mg/kg-1)的作用,即在维拉帕米存在的情况下,高剂量外源性NiCl2增加了CBF和BC。PBZ预处理对镍的CBF降低效果影响不显著。结果表明,微量外源性NiCl2通过增强Ca2+内流到血管平滑肌细胞,而不是由α受体介导,从而诱导犬心脏冠状动脉血管原位收缩。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Effect of verapamil and phenoxybenzamine on nickel-induced coronary vasoconstriction in the anaesthetized dog.

Ni-induced coronary vasoconstriction has been studied in the dog heart in situ in the presence of the selective Ca-antagonist verapamil, and after blocking the alpha-receptors with phenoxybenzamine (PBZ). Verapamil totally abolished the coronary blood flow (CBF) and basal conductance (BC) decreasing effect of low doses of Ni2+ (0.02-0.2 mg/kg-1). The effect of higher doses of Ni2+ (2.0-20.0 mg/kg-1) was reversed by verapamil, i.e. high doses of exogenous NiCl2 increased CBF and BC in the presence of verapamil. The CBF decreasing effect of nickel was not significantly influenced by PBZ pretreatment. The results indicate that trace amounts of exogenous NiCl2 induce coronary vasoconstriction in the dog heart in situ by enhancing Ca2+-influx into vascular smooth muscle cells, which is not mediated by alpha-receptors.

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