SYMPATHETIC AND PARASYMPATHETIC INTERACTIONS UPON LEFT VENTRICLE OF DOG
SYMPATHETIC AND PARASYMPATHETIC INTERACTIONS UPON LEFT VENTRICLE OF DOG
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DOI：
10.1161/01.res.19.1.5
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发表时间：
1966-01-01
影响因子：
20.1
通讯作者：
ZIESKE, H
中科院分区：
文献类型：
--
作者：
LEVY, MN;NG, M;ZIESKE, H
在犬的等容左心室制备中，刺激切断的颈迷走神经的心端引起左心室收缩压（LVSP）的双相变化。典型地，在刺激期间LVSP有明确的降低，然后在停止刺激后LVSP略有增加。当交感神经活动直接增加（通过电刺激左星状神经节）或反射性增加（通过降低颈动脉窦压）时，迷走神经刺激期间LVSP降低的幅度显著增加。这些结果表明，迷走神经刺激的效果是介导的，至少部分地，通过拮抗占主导地位的交感神经活动的正性肌力作用。刺激后反弹的机制尚不清楚。这可能是由于犬迷走交感神经干中的心交感纤维和心肌中释放的儿茶酚胺样物质所致。
In canine, isovolumetric, left ventricle preparations, stimulation of the cardiac end of a cut cervical vagus nerve evokes a biphasic change of left ventricular systolic pressure (LVSP). Characteristically, there is a definite reduction of LVSP during the stimulus, followed by a slight increase of LVSP after cessation of stimulation. The magnitude of the reduction of LVSP during vagal stimulation is considerably augmented when sympathetic activity is increased either directly (by electrical stimulation of the left stellate ganglion) or reflexly (by lowering carotid sinus pressure). These results indicate that the effect of vagal stimulation is mediated, at least in part, by antagonizing the positive inotropic influence of the prevailing sympathetic nervous activity. The mechanism of the poststimulation rebound is unknown. It may be due to cardiac sympathetic fibers in the canine vagosympathetic nerve trunks and to the release of catecholamine-like substances in the myocardium.