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心动过速诱发的犬心力衰竭中,心脏传出交感神经元释放去甲肾上腺素及改变心脏功能的能力降低。

Reduced capacity of cardiac efferent sympathetic neurons to release noradrenaline and modify cardiac function in tachycardia-induced canine heart failure.

作者信息

Cardinal R, Nadeau R, Laurent C, Boudreau G, Armour J A

机构信息

Départment de pharmacologie, Faculté de médecine, Université de Montréal, QC, Canada.

出版信息

Can J Physiol Pharmacol. 1996 Sep;74(9):1070-8.

PMID:8960400
Abstract

To investigate the capacity of efferent sympathetic neurons to modulate the failing heart, stellate ganglion stimulation was performed in dogs with biventricular heart failure induced by rapid ventricular pacing (240 beats/min) for 4-6 weeks. Less noradrenaline was released from cardiac myoneural junctions into coronary sinus blood in response to left stellate ganglion stimulation in anesthetized failing heart preparations (582 pg/mL, lower and upper 95% confidence intervals of 288 and 1174 pg/mL, n = 19) compared with healthy heart preparations (6391 pg/mL, 95% confidence intervals of 4180 and 9770 pg/mL, n = 14; p < 0.001). There was substantial adrenaline extraction by failing hearts (49 +/- 6%), although it was slightly lower than in healthy heart preparations (65 +/- 9%, p = 0.055). In contrast with healthy heart preparations, no net release of adrenaline occurred during stellate ganglion stimulation in any of the failing heart preparations, and ventricular tissue levels of adrenaline fell below the sensitivity limit of the HPLC technique. In failing heart preparations, maximal electrical stimulation of right or left stellate ganglia resulted in minimal augmentation of left ventricular intramyocardial (17%) and chamber (12%) systolic pressures. These indices were augmented by 145 and 97%, respectively, following exogenous noradrenaline administration. Thus, the cardiac efferent sympathetic neurons' reduced capacity to release noradrenaline and modify cardiac function can contribute to reduction of sympathetic support to the failing heart.

摘要

为研究传出性交感神经元调节衰竭心脏的能力,对通过快速心室起搏(240次/分钟)诱导4 - 6周造成双心室心力衰竭的犬进行星状神经节刺激。与健康心脏标本相比,在麻醉的衰竭心脏标本中,左星状神经节刺激后,心肌神经接头释放到冠状窦血中的去甲肾上腺素减少(582 pg/mL,95%置信区间下限和上限分别为288和1174 pg/mL,n = 19),而健康心脏标本为(6391 pg/mL,95%置信区间为4180和9770 pg/mL,n = 14;p < 0.001)。衰竭心脏对肾上腺素的摄取量很大(49±6%),尽管略低于健康心脏标本(65±9%,p = 0.055)。与健康心脏标本不同,在任何衰竭心脏标本中,星状神经节刺激期间均未出现肾上腺素的净释放,且心室组织中的肾上腺素水平降至高效液相色谱技术的检测灵敏度下限以下。在衰竭心脏标本中,右或左星状神经节的最大电刺激导致左心室内心肌收缩压(17%)和心腔收缩压(12%)的增幅最小。在外源性给予去甲肾上腺素后,这些指标分别增加了145%和97%。因此,心脏传出性交感神经元释放去甲肾上腺素及改变心脏功能的能力降低,可能导致对衰竭心脏的交感支持减少。

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