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首页> 外文期刊>The Korean Journal of Physiology & Pharmacology >Influence of Ketamine on Catecholamine Secretion in the Perfused Rat Adrenal Medulla
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Influence of Ketamine on Catecholamine Secretion in the Perfused Rat Adrenal Medulla

机译：氯胺酮对灌注大鼠肾上腺髓质中儿茶酚胺分泌的影响

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摘要

The aim of the present study was to examine the effects of ketamine, a dissociative anesthetics, on secretion of catecholamines (CA) secretion evoked by cholinergic stimulation from the perfused model of the isolated rat adrenal gland, and to establish its mechanism of action, and to compare ketamine effect with that of thiopental sodium, which is one of intravenous barbiturate anesthetics. Ketamine (30~300μM), perfused into an adrenal vein for 60 min, dose- and time-dependently inhibited the CA secretory responses evoked by ACh (5.32 mM), high K+ (a direct membrane-depolarizer, 56 mM), DMPP (a selective neuronal nicotinic NN receptor agonist, 100μM) and McN-A-343 (a selective muscarinic M1 receptor agonist, 100μM). Also, in the presence of ketamine (100μM), the CA secretory responses evoked by veratridine (a voltage-dependent Na+ channel activator, 100μM), Bay-K-8644 (an L-type dihydropyridine Ca2+ channel activator, 10μM), and cyclopiazonic acid (a cytoplasmic Ca2+-ATPase inhibitor, 10μM) were significantly reduced, respectively. Interestingly, thiopental sodium (100μM) also caused the inhibitory effects on the CA secretory responses evoked by ACh, high K+ , DMPP, McN-A-343, veratridine, Bay-K-8644, and cyclopiazonic acid. Collectively, these experimental results demonstrate that ketamine inhibits the CA secretion evoked by stimulation of cholinergic (both nicotinic and muscarinic) receptors and the membrane depolarization from the isolated perfused rat adrenal gland. It seems likely that the inhibitory effect of ketamine is mediated by blocking the influx of both Ca2+ and Na+ through voltage-dependent Ca2+ and Na+ channels into the rat adrenal medullary chromaffin cells as well as by inhibiting Ca2+ release from the cytoplasmic calcium store, which are relevant to the blockade of cholinergic receptors. It is also thought that, on the basis of concentrations, ketamine causes similar inhibitory effect with thiopental in the CA secretion from the perfused rat adrenal medulla.
机译：本研究的目的是研究氯胺酮（一种解离性麻醉药）对离体大鼠肾上腺灌注模型中胆碱能刺激引起的儿茶酚胺（CA）分泌的影响，并建立其作用机理，以及比较氯胺酮和硫喷妥钠的作用，后者是静脉注射巴比妥酸盐麻醉剂之一。氯胺酮（30〜300μM）注入肾上腺静脉60分钟，剂量和时间依赖性抑制ACh（5.32 mM），高K + （直接膜去极化剂56 mM），DMPP（选择性神经元烟碱NN受体激动剂，100μM）和McN-A-343（选择性毒蕈碱M1受体激动剂，100μM）。同样，在存在氯胺酮（100μM）的情况下，维拉替丁（电压依赖性Na + 通道激活剂，100μM），Bay-K-8644（L型二氢吡啶分别显着降低了 2 + 通道激活剂（10μM）和环吡嗪酸（一种细胞质Ca 2 + -ATPase抑制剂，10μM）。有趣的是，硫喷妥钠（100μM）也对ACh，高K + ，DMPP，McN-A-343，veratridine，Bay-K-8644和环吡唑酮引起的CA分泌反应产生抑制作用。酸。总的来说，这些实验结果表明，氯胺酮抑制了胆碱能（烟碱和毒蕈碱）受体的刺激以及从离体灌流的大鼠肾上腺的膜去极化引起的CA分泌。氯胺酮的抑制作用似乎是通过抑制电压依赖性Ca 2 + 和Na + 的流入而介导的>和Na + 通道进入大鼠肾上腺髓质嗜铬细胞，并通过抑制Ca 2 + 从细胞质钙库释放，这与胆碱能受体的阻断有关。还认为，基于浓度，氯胺酮在从灌注的大鼠肾上腺髓质的CA分泌中引起与硫喷妥钠相似的抑制作用。

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