Vagus Nerves and Baroreceptor Control of Ventricular Performance
Vagus Nerves and Baroreceptor Control of Ventricular Performance
复制标题
迷走神经和压力感受器对心室性能的控制
作者：
M. N. Levy;M. Ng;R. I. Lipman;H. Zieske
在神经支配，等容左心室准备，突然升高的压力在孤立的颈动脉窦引起了9.5%的左心室收缩压（LVSP）的抑郁症。用甲苯磺酸溴苄铵阻断交感神经效应器接头后，相当于窦内压力变化引起LVSP降低6.8%。硫酸阿托品或冷却颈迷走神经可完全消除这种反应。因此，在本实验的条件下，迷走神经介导了颈动脉窦压力感受器刺激引起的心室性能的反射抑制的显著部分。阻断交感神经连接后，阿托品和迷走神经冷却可使LVSP明显升高。这种心室功能的增强表明迷走神经对心室心肌有紧张性负性肌力作用。
In innervated, isovolumetric left ventricle preparations, sudden elevations of pressure in the isolated carotid sinus elicited a 9.5% depression of left ventricular systolic pressure (LVSP). After blockade of sympathetic neuroeffector junctions by bretylium tosylate, equivalent intrasinusal pressure changes evoked a 6.8% reduction of LVSP. This response could be completely abolished by atropine sulfate or by cooling the cervical vagi. Therefore, under the conditions of the present experiments, the vagus nerves mediated a significant fraction of the reflex depression of ventricular performance induced by carotid sinus baroreceptor stimulation. An appreciable elevation of LVSP was produced by atropine and by vagal cooling after blockade of sympathetic junctions. This enhancement of ventricular performance is an indication of a tonic negative inotropic influence of the vagus nerves upon the ventricular myocardium.