Either desipramine or TMB-8 suppresses cyanide-induced norepinephrine efflux from in vivo cardiac sympathetic nerves of cats
Either desipramine or TMB-8 suppresses cyanide-induced norepinephrine efflux from in vivo cardiac sympathetic nerves of cats
复制标题
地昔帕明或 TMB-8 抑制氰化物诱导的猫体内心脏交感神经去甲肾上腺素外流
DOI：
10.1016/s0006-8993(00)02176-4
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发表时间：
2000
期刊：
影响因子：
2.9
通讯作者：
T. Akiyama
中科院分区：
文献类型：
--
作者：
N. Yahagi;T. Yamazaki;T. Akiyama
为探讨缺氧对心脏交感神经末梢内源性去甲肾上腺素（NE）释放的影响，我们通过透析探头将氰化钠（NaCN）注入心肌间质30 min，并测量透析液NE水平。在NaCN灌注期间，观察到透析液NE显著且浓度依赖性增加。这种氰化物诱导的NE反应被地匹胺（一种膜性NE转运抑制剂）预处理抑制。此外，TMB-8（胞内Ca ~（2+）拮抗剂）预处理可抑制氰化物诱导的NE反应，而NE释放抑制剂ω-芋螺毒素GVIA（NE释放抑制剂）对NE反应无影响。我们的数据表明，两个（地昔帕明或TMB-8抑制）机制有助于在体内心脏交感神经的NE流出量的氰化物诱导。
To investigate the effect of hypoxia on endogenous norepinephrine (NE) release from cardiac sympathetic nerve ending, we administered sodium cyanide (NaCN) for 30 min into the myocardial interstitial space through a dialysis probe and measured dialysate NE levels. During the NaCN perfusion, a marked and concentration-dependent increase in dialysate NE was observed. This cyanide-induced NE response was suppressed by pretreatment with despiramine (a membraneous NE transport inhibitor). Furthermore, the cyanide-induced NE response was suppressed by pretreatment with TMB-8 (intracellular Ca2+antagonist) but unaffected by ω-conotoxin GVIA (NE releasing inhibitor). Our data suggest that two (desipramine or TMB-8 suppressive) mechanisms contributed to the amount of NE efflux induced by cyanide in in vivo cardiac sympathetic nerve.
影响因子：
15.9
作者：
TETI, A;BLAIR, HC;HRUSKA, KA
通讯作者：
HRUSKA, KA
冠状动脉植入术后交感神经激活的收缩反应。
DOI：
10.1152/ajpheart.1987.252.6.h1059
发表时间：
1987
期刊：
The American journal of physiology
影响因子：
--
作者：
Heusch,G;Guth,BD;Roth,DM;Seitelberger,R;RossJr,J
通讯作者：
RossJr,J