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哇巴因可增强单侧迷走神经刺激诱发的心脏乙酰胆碱释放。

Ouabain enhances release of acetylcholine in the heart evoked by unilateral vagal stimulation.

作者信息

Feinauer M, Lindmar R, Löffelholz K, Ullrich B

出版信息

Naunyn Schmiedebergs Arch Pharmacol. 1986 May;333(1):7-12. doi: 10.1007/BF00569652.

Abstract

The aim of the study was to elucidate peripheral effects of ouabain on the parasympathetic innervation of the heart, effects that could contribute to the experimentally and clinically well established "vagal effect of cardiac glycosides". The experiments were carried out with ouabain concentrations of 3 X 10(-7) and 10(-6) mol/l, which were considered "therapeutic", as they increased force of contraction and did not elicit arrhythmias in incubated chicken atria. In atrial preparations of chickens and guinea-pigs the negative chronotropic and inotropic effects of acetylcholine (ACh) were not altered by 3 X 10(-7) mol/l ouabain. Resting efflux of ACh from perfused chicken hearts was increased by ouabain from 10 to a maximum of 30 pmol/g min, whereas release of ACh evoked by bilateral vagal stimulation at 3 or 20 Hz for 1 min was unchanged (resting release subtracted). In contrast, release of ACh caused by unilateral vagal stimulation was augmented by ouabain up to 200% of the control. Release by unilateral stimulation (80 pmol/g; 20 Hz) was calculated for each experiment by averaging the releases evoked by consecutive stimulation of the right and left nerves. Ouabain infused for 90 min did not alter the tissue content of ACh (5.5 nmol/g). Within 2 days after unilateral (left) vagal transsection (denervation of cardiac ganglia) the release of ACh evoked by stimulation of the intact nerve (20 Hz) increased from about 80 to 200 pmol/g, whereas the release from the lesioned nerve markedly declined.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

该研究的目的是阐明哇巴因对心脏副交感神经支配的外周作用,这些作用可能有助于实验和临床上已充分证实的“强心苷的迷走神经效应”。实验采用的哇巴因浓度为3×10⁻⁷和10⁻⁶mol/L,这两个浓度被认为是“治疗浓度”,因为它们能增加收缩力,且在孵育的鸡心房中不会引发心律失常。在鸡和豚鼠的心房制备物中,3×10⁻⁷mol/L的哇巴因不会改变乙酰胆碱(ACh)的负性变时和变力作用。哇巴因可使灌注鸡心脏中ACh的静息流出量从10增加到最大30 pmol/g·min,而双侧迷走神经以3或20 Hz刺激1分钟所诱发的ACh释放量不变(减去静息释放量)。相比之下,哇巴因可使单侧迷走神经刺激所引起的ACh释放量增加至对照的200%。每次实验中,单侧刺激(80 pmol/g;20 Hz)所引起的释放量通过对左右神经连续刺激所诱发的释放量求平均值来计算。输注90分钟的哇巴因不会改变ACh的组织含量(5.5 nmol/g)。在单侧(左侧)迷走神经横断(心脏神经节去神经支配)后2天内,刺激完整神经(20 Hz)所诱发的ACh释放量从约80增加到200 pmol/g,而损伤神经的释放量则明显下降。(摘要截取自250字)

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