Inhibitory effects of nicorandil on sympathetic coronary vasoconstriction.

Inhibitory effects of nicorandil on sympathetic coronary vasoconstriction.
复制标题

尼可地尔对交感冠状动脉血管收缩的抑制作用。

DOI:
10.1093/cvr/28.6.917
复制
发表时间:
1994
影响因子:
10.8
通讯作者:
H. Okino
H. Okino
中科院分区:
医学1区
文献类型:
--
作者:
M. Chujo;H. Mori;E. Tanaka;H. Nakazawa;H. Okino

文献摘要

被引文献

相似文献

客观化 目的是研究尼可地尔是否能抑制刺激交感神经供应到心脏时冠状动脉血管阻力的增加,如果是的话,作用机制是什么。 方法 采用β受体阻断法,观察尼可地尔对心脏腹外侧部神经刺激时冠脉阻力的影响,以及对冠脉内注入去甲肾上腺素或神经肽Y(NPY)的反应性的影响。本文比较了尼可地尔对刺激锁骨下动脉时去甲肾上腺素和神经肽Y溢出的影响,并与对照组和切断迷走神经同时阻断α和β受体阻断剂L组进行了比较。 结果 冠状动脉内输注尼可地尔可在心神经刺激前降低冠脉血管阻力,在刺激期间,尼可地尔抑制从刺激前的阻力增加的百分比。尼可地尔抑制冠脉血管对外源性去甲肾上腺素和神经肽Y的反应性。在20赫兹刺激锁骨下动脉时,心房内注入尼可地尔可显著减少NPY的溢出,但不能减少去甲肾上腺素的溢出。硝酸甘油+L-NNA组未见此抑制作用。 结论 尼可地尔通过降低血管对交感神经递质的反应性和抑制心脏交感神经刺激期间NPY的溢出来减少交感神经冠状动脉的收缩。对NPY溢出的抑制作用被认为是由于交感神经末梢上的ATP敏感性钾通道的开放,而不是尼可地尔的硝酸甘油样作用。
OBJECTIVE The aim was to investigate whether nicorandil suppresses the rise in coronary vascular resistance that occurs during stimulation of the sympathetic nerve supply to the heart and, if so, what are the mechanisms of action. METHODS The effects of nicorandil on coronary vascular resistance during ventrolateral cardiac nerve stimulation and on the reactivity of the coronary vasculature to intracoronary infusion of noradrenaline or neuropeptide Y (NPY) were examined under beta receptor blockade. The effects of nicorandil on the overflow of noradrenaline and NPY during ansae subclaviae stimulation were compared with those in a control group and in a group treated with glyceryl trinitrate and N omega-nitro-L-arginine (L-NNA) under both alpha and beta receptor blockade with vagotomy. RESULTS Intracoronary infusion of nicorandil decreased coronary vascular resistance prior to cardiac nerve stimulation, and during stimulation it suppressed the percentage increase in resistance from the prestimulation value. Nicorandil suppressed the reactivity of the coronary vasculature to exogenous noradrenaline and NPY. Intra-atrial infusion of nicorandil significantly reduced the overflow of NPY but not of noradrenaline during stimulation of the ansae subclaviae at 20 Hz. This suppressive effect was not observed in the glyceryl trinitrate + L-NNA group. CONCLUSIONS Nicorandil reduces sympathetic coronary vasoconstriction by decreasing the reactivity of the vasculature to sympathetic neurotransmitters and by suppressing NPY overflow during cardiac sympathetic nerve stimulation. The suppressive action on NPY overflow is thought to be due to the opening of ATP sensitive potassium channels in the sympathetic nerve endings rather than to a glyceryl trinitrate-like action of nicorandil.