烟酸或烟酰胺对代谢性冠状动脉血管舒张的增强作用。

Enhancement of metabolic coronary vasodilatation by nicotinic acid or amide.

作者信息

Talesnik J, Labelle S

出版信息

Pharmacol Res Commun. 1984 Mar;16(3):253-63. doi: 10.1016/s0031-6989(84)80108-3.

Abstract

Cardiostimulation produced by noradrenaline, glucagon, or tachycardia on the isolated perfused rat heart produced a metabolic coronary dilatation that was potentiated by nicotinic acid or its amide [NIC; 0.05-1.0 mM] without affecting the cardiostimulation. Reactive hyperaemia to brief coronary occlusion was unaffected by NIC, thus confirming that its vasodilator mechanism is of a different nature than that leading to metabolic coronary dilatation. It is suggested that NIC may be of significance as an adjuvant in the treatment of certain types of coronary insufficiencies.

摘要

去甲肾上腺素、胰高血糖素或心动过速对离体灌注大鼠心脏产生的心脏刺激会引发代谢性冠状动脉扩张，烟酸或其酰胺[NIC；0.05 - 1.0 mM]可增强这种扩张，且不影响心脏刺激。NIC对短暂冠状动脉闭塞引起的反应性充血无影响，从而证实其血管舒张机制与导致代谢性冠状动脉扩张的机制性质不同。有人提出，NIC作为辅助药物在某些类型的冠状动脉功能不全治疗中可能具有重要意义。